You searched for subject:(Fibroblast Growth Factor)
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University of Hawaii – Manoa
1.
Ulu, Ferhat.
Dose-dependent functions of FGF9 in male primordial germ cell differentiation.
Degree: 2016, University of Hawaii – Manoa
URL: http://hdl.handle.net/10125/100649
► M.S. University of Hawaii at Manoa 2013.
Primordial Germ Cells (PGCs) are the precursors of gametes. For PGC male differentiation, (i) inhibition of meiosis and…
(more)
▼ M.S. University of Hawaii at Manoa 2013.
Primordial Germ Cells (PGCs) are the precursors of gametes. For PGC male differentiation, (i) inhibition of meiosis and (ii) male-inducing factor(s) are essential. It was recently revealed that Fibroblast Growth Factor 9 (FGF9) is one of male-inducing factors. Using isolated PGC culture system, we examined the function of FGF9 in PGC differentiation. We found low FGF9 treatment (0.2 ng/ml) induced PGC male differentiation. Conversely, high FGF9 treatment drastically stimulated PGC proliferation (40%) compared with the control and low FGF9 groups (5~10%). As a result, high FGF9 treatment (25 ng/ml) prevented PGCs to enter the male pathway. Also, we demonstrated that high FGF9 induced ERK1/2 signaling activation for stimulating PGC proliferation while low FGF9 enhanced phosphorylation of p38 signaling to push PGCs into the male pathway.
Subjects/Keywords: Fibroblast Growth Factor 9
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APA (6th Edition):
Ulu, F. (2016). Dose-dependent functions of FGF9 in male primordial germ cell differentiation. (Thesis). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/100649
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ulu, Ferhat. “Dose-dependent functions of FGF9 in male primordial germ cell differentiation.” 2016. Thesis, University of Hawaii – Manoa. Accessed April 18, 2021.
http://hdl.handle.net/10125/100649.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ulu, Ferhat. “Dose-dependent functions of FGF9 in male primordial germ cell differentiation.” 2016. Web. 18 Apr 2021.
Vancouver:
Ulu F. Dose-dependent functions of FGF9 in male primordial germ cell differentiation. [Internet] [Thesis]. University of Hawaii – Manoa; 2016. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/10125/100649.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ulu F. Dose-dependent functions of FGF9 in male primordial germ cell differentiation. [Thesis]. University of Hawaii – Manoa; 2016. Available from: http://hdl.handle.net/10125/100649
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center
2.
Kir, Serkan.
Regulation of Liver Metabolism by Fibroblast Growth Factor 19.
Degree: 2012, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/1027
► Fibroblast Growth Factor (FGF) 19 is a postprandial enterokine up-regulated by bile acid receptor FXR upon bile acid uptake into the ileum. FGF19 inhibits hepatic…
(more)
▼ Fibroblast Growth Factor (FGF) 19 is a postprandial enterokine up-regulated by bile acid receptor FXR upon bile acid uptake into the ileum. FGF19 inhibits hepatic bile acid synthesis through transcriptional repression of cholesterol 7 alpha-hydroxylase (CYP7A1) via a mechanism involving nuclear receptor Small Heterodimer Partner (SHP). Here, I show that two other nuclear receptors, Hepatocyte Nuclear
Factor 4 alpha (HNF4 alpha) and Liver Receptor Homolog-1 (LRH-1), enable SHP binding to the Cyp7a1 promoter and therefore are important for negative feedback regulation of Cyp7a1. HNF4 alpha and LRH-1 are also crucial activators of Cyp7a1 transcription. They maintain active transcription histone marks on the Cyp7a1 promoter, whereas FGF19 down-regulates these marks in a SHP-dependent way.
Secondly, I show that the MEK/ERK signaling pathway is an integral regulator of bile acid metabolism. ERK activity is necessary to maintain hepatic Shp and Cyp7a1 transcription at their physiologic levels. Inhibition of this pathway causes loss of Shp transcription by disrupting HNF4 alpha and LRH-1 binding to the Shp promoter. Independent from the effects on Shp, MEK/ERK inhibition induces Cyp7a1 transcription. Unexpectedly, the MEK/ERK pathway is not required for repression of Cyp7a1 by FGF19. Although this pathway is activated by FGF19 in livers of Fgf receptor 4 (Fgfr4)-deficient mice probably via other FGFRs, Cyp7a1 repression is largely impaired. Thus, I propose that a signaling mechanism uniquely regulated by FGFR4 must be responsible for FGF19-dependent repression of bile acid synthesis.
In addition to its roles in bile acid metabolism, I also show that FGF19 stimulates hepatic protein and glycogen synthesis, but does not induce lipogenesis. The effects of FGF19 are independent of the activity of either insulin or the protein kinase Akt, and instead are mediated through a mitogen-activated protein kinase signaling pathway that activates components of the protein translation machinery and stimulates glycogen synthase activity. Mice lacking FGF15 (the mouse FGF19 ortholog) fail to properly regulate blood glucose and fail to maintain normal postprandial amounts of liver glycogen. FGF19 treatment restored the loss of glycogen in diabetic animals lacking insulin. Thus, FGF19 activates a physiologically important, insulin-independent endocrine pathway that regulates hepatic protein and glycogen metabolism.
Advisors/Committee Members: Mangelsdorf, David J., Kliewer, Steven A..
Subjects/Keywords: Liver Glycogen; Fibroblast Growth Factor; Protein Biosynthesis
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APA ·
Chicago ·
MLA ·
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CSE |
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APA (6th Edition):
Kir, S. (2012). Regulation of Liver Metabolism by Fibroblast Growth Factor 19. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1027
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kir, Serkan. “Regulation of Liver Metabolism by Fibroblast Growth Factor 19.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed April 18, 2021.
http://hdl.handle.net/2152.5/1027.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kir, Serkan. “Regulation of Liver Metabolism by Fibroblast Growth Factor 19.” 2012. Web. 18 Apr 2021.
Vancouver:
Kir S. Regulation of Liver Metabolism by Fibroblast Growth Factor 19. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2152.5/1027.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kir S. Regulation of Liver Metabolism by Fibroblast Growth Factor 19. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1027
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center
3.
Bookout, Angie Lynn.
The Liver-Derived Endocrine Hormone FGF21 Alters Metabolism and Diurnal Behavior via the Nervous System.
Degree: 2012, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/987
► Fuel acquisition is essential to survival. During privation, the body protects glucose concentrations acutely by glycogenolysis, and later by gluconeogenesis and ketogenesis. Additionally, animals alter…
(more)
▼ Fuel acquisition is essential to survival. During privation, the body protects glucose concentrations acutely by glycogenolysis, and later by gluconeogenesis and ketogenesis. Additionally, animals alter daily behavioral patterns to seek food, but eventually reduce energetically costly activities (
growth, reproduction, locomotion). Little is known about the mechanisms that orchestrate and coordinate these physiological and behavioral responses to starvation. The liver-derived endocrine hormone
fibroblast growth factor 21 (FGF21) is induced in chronic fasting and acts as a global starvation signal. Previous studies focusing on FGF21 as an anti-diabetic drug indicate that FGF21 coordinates whole-body fat utilization and energy expenditure. However, its basic physiological role is underexplored.
Acute injection of recombinant FGF21 quickly elicits a coordinated program between tissues resulting in reduced plasma insulin and gluconeogenic and thermogenic gene expression programs in liver and brown adipose, effects that require an intact animal. Mice with chronic FGF21 overexpression (FGF21tg) are smaller in size, females are infertile, and if fasted, they undergo torpor, an energy-conserving process. Taken together, these data suggest that FGF21 may exert some effects through the nervous system.
To explore this idea, I utilized anatomically-guided laser capture microdissection followed by quantitative, real-time PCR to profile expression of the FGF receptor/co-receptor family in specific hypothalamic nuclei of mice. Surprisingly, the FGFR1-IIIc/βKlotho complex is found in the suprachiasmatic nucleus (SCN), area postrema (AP), nucleus tractus solitarii (NTS), and nodose ganglion (cell body of vagus nerve), implicating roles in circadian and metabolic regulation.
Results of surgical, pharmacological, and genetic strategies indicate the vagus senses circulating FGF21, resulting in adrenergic efferent responses that reduce insulin secretion, while a different adrenergic site modulates liver and brown adipose gene expression.
Analyses of the effects of FGF21 on the SCN, the body’s master clock, using running wheels show FGF21tg mice have dramatically altered circadian activity, likely as a consequence of inhibiting SCN output functions. Deletion of βKlotho specifically from the SCN rescues this behavior in addition to
growth defects of FGF21tg mice.
To date, this is the first description of a liver-derived endocrine hormone that affects such diverse aspects of the starvation response by acting on the nervous system.
Advisors/Committee Members: Mangelsdorf, David J..
Subjects/Keywords: Fibroblast Growth Factor; PPAR gamma; Liver
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bookout, A. L. (2012). The Liver-Derived Endocrine Hormone FGF21 Alters Metabolism and Diurnal Behavior via the Nervous System. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/987
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Bookout, Angie Lynn. “The Liver-Derived Endocrine Hormone FGF21 Alters Metabolism and Diurnal Behavior via the Nervous System.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed April 18, 2021.
http://hdl.handle.net/2152.5/987.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Bookout, Angie Lynn. “The Liver-Derived Endocrine Hormone FGF21 Alters Metabolism and Diurnal Behavior via the Nervous System.” 2012. Web. 18 Apr 2021.
Vancouver:
Bookout AL. The Liver-Derived Endocrine Hormone FGF21 Alters Metabolism and Diurnal Behavior via the Nervous System. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2152.5/987.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Bookout AL. The Liver-Derived Endocrine Hormone FGF21 Alters Metabolism and Diurnal Behavior via the Nervous System. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/987
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign
4.
Camero, Corrine Michelle.
Investigating fibroblast growth factor and its role in canine osteosarcoma.
Degree: MS, VMS-Veterinary Clinical Medcne, 2017, University of Illinois – Urbana-Champaign
URL: http://hdl.handle.net/2142/99310
► Canine osteosarcoma (OS) is a malignant neoplasia of the osteoblast, most often identified in the appendicular skeleton, which is both locally aggressive and highly metastatic.…
(more)
▼ Canine osteosarcoma (OS) is a malignant neoplasia of the osteoblast, most often identified in the appendicular skeleton, which is both locally aggressive and highly metastatic. The standard of care treatment of amputation and adjuvant chemotherapy yields a median survival time of 10-12 months, an improvement in which has not been noted despite active research. The biologic behavior of cancers seems to be correlated to the state of differentiation of the tumor cell population. Differentiation is taken into account when a histopathologic grade is assigned to a particular tumor; poorly differentiated tumors acquire a higher grade and are expected to behave more aggressively. The tumor microenvironment contains many cells and signaling molecules such as cytokines, chemokines and
growth factors. Investigating these factors may identify a stimulus for a less differentiated and more aggressive neoplasia. This is even more compelling if the stimulus is a druggable target.
Fibroblast growth factors (FGFs) interact with
fibroblast growth factor receptors (FGFRs) to initiate cell signaling that is important in embryonic development, wound healing, and angiogenesis. FGF2, also termed basic FGF (bFGF), plays an important role in osteoblast proliferation and maintaining osteoblasts in an undifferentiated state.
We hypothesize that 1) canine OS cells will express FGFRs and FGF2, 2) FGF signaling blockade will attenuate pro-tumorigenic properties in OS cells, 3) FGF signaling blockade will cause enhanced differentiation of the OS cell lines, and 4) circulating FGF2 will be increased in canine OS patients compared to healthy controls and increased in dogs with osteoblastic OS compared to those with osteolytic OS.
We investigated FGFR gene expression with reverse transcriptase polymerase chain reaction (RT-PCR) and FGF2 secretion via ELISA. The effects of FGF signaling attenuation on OS cell pro-tumorigenic properties were evaluated by colorimetric proliferation assay and scratch migration assay. The effects of FGF signaling blockade with pan-FGFR inhibitor BGJ398 on OS cell differentiation were evaluated with Alizarin Red staining and quantification, alkaline phosphatase (ALP) bio-activity, and quantitative real time reverse transcription polymerase chain reaction (qRT-PCR) for osteogenic genes alkaline phosphatase (ALP), osterix(OSTX), osteonectin (OSN), and runt-related transcription
factor 2 (RUNX2). Circulating FGF2 levels were quantified in the plasma of dogs with naturally occurring OS (determined to be osteoblastic or osteolytic based on relative bone mineral density obtained via DEXA scan) and healthy controls via ELISA.
FGFR gene expression was noted in OS cell lines. FGF2 secretion was identified in all cell lines with secretion noted in a clear cell density-dependent manner in 2 of 3 cell lines. FGFR signaling attenuation inhibited OS cell migration while not affecting cell proliferation. FGFR signaling blockade increased differentiation in 1 of 2 cell lines evaluated, with a trend toward increased differentiation in…
Advisors/Committee Members: Fan, Timothy M (advisor), Stewart, Matthew (committee member), Selmic, Laura (committee member).
Subjects/Keywords: fibroblast growth factor; canine osteosarcoma; differentiation
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Camero, C. M. (2017). Investigating fibroblast growth factor and its role in canine osteosarcoma. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/99310
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Camero, Corrine Michelle. “Investigating fibroblast growth factor and its role in canine osteosarcoma.” 2017. Thesis, University of Illinois – Urbana-Champaign. Accessed April 18, 2021.
http://hdl.handle.net/2142/99310.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Camero, Corrine Michelle. “Investigating fibroblast growth factor and its role in canine osteosarcoma.” 2017. Web. 18 Apr 2021.
Vancouver:
Camero CM. Investigating fibroblast growth factor and its role in canine osteosarcoma. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2017. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2142/99310.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Camero CM. Investigating fibroblast growth factor and its role in canine osteosarcoma. [Thesis]. University of Illinois – Urbana-Champaign; 2017. Available from: http://hdl.handle.net/2142/99310
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Louisiana State University
5.
Sutton, Elizabeth Frost.
Fibroblast Growth Factor 21 is a Novel Protein Sensor in Pregnancy.
Degree: PhD, Life Sciences, 2017, Louisiana State University
URL: etd-05182017-213436
;
https://digitalcommons.lsu.edu/gradschool_dissertations/4263
► The twenty-first century has experienced a shift in cause of death worldwide from communicable diseases to noncommunicable diseases. Interestingly, many of these implicated chronic diseases,…
(more)
▼ The twenty-first century has experienced a shift in cause of death worldwide from communicable diseases to noncommunicable diseases. Interestingly, many of these implicated chronic diseases, such as cancer, diabetes, and cardiovascular disease, have been shown to be programmed in the womb. As first posited by the Barker Hypothesis, adverse exposures in utero can increase an individual’s risk for chronic disease later in life. Therefore, pregnancy is an opportune time for intervention to improve the health of future generations. Studies of exposures known to negatively impact infant health, e.g. states of overnutrition (obesity, diabetes, excess gestational weight gain) and undernutrition (starvation, protein restriction), are critical to reveal the mechanisms of and identify markers for developmental programming. Numerous endocrine signals including insulin, leptin, and adiponectin have been extensively investigated during pregnancy with aberrant effects on offspring growth and metabolic function. A novel endocrine hormone, fibroblast growth factor 21 (FGF21), which has been recently implicated as a signal for protein restriction, has not yet been studied for a potential role in developmental programming of future disease. Therefore, we aimed to investigate the role of FGF21 in pregnancy. We hypothesized FGF21 may be a nutrient sensor and a signal for fetal nutrient insufficiency during pregnancy. In studies of healthy, pregnant women, we found FGF21 was acutely regulated by maternal macronutrient balance. We then found in both mice and human studies that FGF21 is elevated in response to low maternal protein intake in pregnancy. We also showed elevated maternal FGF21 correlated with decreased infant size in the first year of life, an outcome commonly associated with reduced maternal protein intake in pregnancy. Finally, we used the Protein Leverage Hypothesis to directly test whether FGF21 is indeed a protein sensor in pregnancy and found that FGF21 is required for the hyperphagic response to low protein intake in pregnancy. In summary, these studies support the hypothesis that FGF21 is a protein sensor in pregnancy. Further studies in large clinical populations including fetal growth restriction are needed to discern whether FGF21 could be used as a marker for fetal nutrient insufficiency in the public health setting.
Subjects/Keywords: Fibroblast growth factor 21; FGF21; pregnancy; protein
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Sutton, E. F. (2017). Fibroblast Growth Factor 21 is a Novel Protein Sensor in Pregnancy. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-05182017-213436 ; https://digitalcommons.lsu.edu/gradschool_dissertations/4263
Chicago Manual of Style (16th Edition):
Sutton, Elizabeth Frost. “Fibroblast Growth Factor 21 is a Novel Protein Sensor in Pregnancy.” 2017. Doctoral Dissertation, Louisiana State University. Accessed April 18, 2021.
etd-05182017-213436 ; https://digitalcommons.lsu.edu/gradschool_dissertations/4263.
MLA Handbook (7th Edition):
Sutton, Elizabeth Frost. “Fibroblast Growth Factor 21 is a Novel Protein Sensor in Pregnancy.” 2017. Web. 18 Apr 2021.
Vancouver:
Sutton EF. Fibroblast Growth Factor 21 is a Novel Protein Sensor in Pregnancy. [Internet] [Doctoral dissertation]. Louisiana State University; 2017. [cited 2021 Apr 18].
Available from: etd-05182017-213436 ; https://digitalcommons.lsu.edu/gradschool_dissertations/4263.
Council of Science Editors:
Sutton EF. Fibroblast Growth Factor 21 is a Novel Protein Sensor in Pregnancy. [Doctoral Dissertation]. Louisiana State University; 2017. Available from: etd-05182017-213436 ; https://digitalcommons.lsu.edu/gradschool_dissertations/4263
6.
Kato, Manabu.
Activation of FGF2-FGFR Signaling in the Castrated Mouse Prostate Stimulates the Proliferation of Basal Epithelial Cells.
Degree: 博士(医学), 2017, Mie University / 三重大学
URL: http://hdl.handle.net/10076/00016972
► The prostate gland is unique in that it undergoes rapid regression following castration but regenerates completely once androgens are replaced. Residual ductal components play an…
(more)
▼ The prostate gland is unique in that it undergoes rapid regression following castration but regenerates completely once androgens are replaced. Residual ductal components play an important role in the regeneration of a fully functional prostate. In this study, to examine how androgen status affects prostate structure and components, we conducted histopathological studies of the involuted and regenerated mouse dorsolateral prostate (DLP). In the castrated mouse DLP, the number of luminal epithelial cells decreased in a time-dependent manner. On Day 14 postandrogen replacement, the number of luminal epithelial cells was completely restored to the baseline level. In contrast, the number of basal epithelial cells gradually increased in the castrated mouse prostate. The Ki67-labeling index of prostate basal epithelial cells was significantly increased after castration. The number of basal epithelial cells decreased to baseline after androgen replacement. After castration, mRNA expression levels of specific growth factors, such as Fgf2, Fgf7, Hgf, Tgfa, and Tgfb, were relatively abundant in whole mouse DLPs. In organ culture experiments, basal epithelial proliferation was recapitulated in the absence of dihydrotestosterone (DHT). The proliferation of basal epithelial cells in the absence of DHT was suppressed by treatment with an FGF receptor inhibitor (PD173074). Moreover, FGF2 treatment directly stimulated the proliferation of basal epithelial cells. Taken together, these data indicated that the FGF2-FGF receptor signal cascade in the prostate gland may be one of the pathways stimulating the proliferation of basal epithelial cells in the absence of androgens. basal epithelial cells, castration, fibroblast growth factor 2, fibroblast growth factor receptor, growth factor, organ culture, prostate
本文 / Department of Nephro-Urologic Surgery and Andrology, Mie University Graduate School of Medicine
10p
Subjects/Keywords: basal epithelial cells; castration; fibroblast growth factor 2; fibroblast growth factor receptor; growth factor; organ culture; prostate
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kato, M. (2017). Activation of FGF2-FGFR Signaling in the Castrated Mouse Prostate Stimulates the Proliferation of Basal Epithelial Cells. (Thesis). Mie University / 三重大学. Retrieved from http://hdl.handle.net/10076/00016972
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kato, Manabu. “Activation of FGF2-FGFR Signaling in the Castrated Mouse Prostate Stimulates the Proliferation of Basal Epithelial Cells.” 2017. Thesis, Mie University / 三重大学. Accessed April 18, 2021.
http://hdl.handle.net/10076/00016972.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kato, Manabu. “Activation of FGF2-FGFR Signaling in the Castrated Mouse Prostate Stimulates the Proliferation of Basal Epithelial Cells.” 2017. Web. 18 Apr 2021.
Vancouver:
Kato M. Activation of FGF2-FGFR Signaling in the Castrated Mouse Prostate Stimulates the Proliferation of Basal Epithelial Cells. [Internet] [Thesis]. Mie University / 三重大学; 2017. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/10076/00016972.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kato M. Activation of FGF2-FGFR Signaling in the Castrated Mouse Prostate Stimulates the Proliferation of Basal Epithelial Cells. [Thesis]. Mie University / 三重大学; 2017. Available from: http://hdl.handle.net/10076/00016972
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
7.
Moore, Lisa.
FGF signaling in Xenopus laevis lens regeneration.
Degree: PhD, Cell and Developmental Biology, 2015, University of Illinois – Urbana-Champaign
URL: http://hdl.handle.net/2142/78759
► The larvae of the frog Xenopus laevis is capable of regenerating lenses. In this re- generative process, the corneal tissue is capable of forming a…
(more)
▼ The larvae of the frog Xenopus laevis is capable of regenerating lenses. In this re- generative process, the corneal tissue is capable of forming a lens after removal of the original lens, but the molecular mechanisms for this process is unknown. This dissertation examines the relationship between FGF signaling and lens regeneration, exploring the hypothesis that the FGF signaling plays a key role in triggering lens regeneration. First, the mRNA expression levels of FGFs and FGFRs in the cornea and retina were observed, as the key ligand from the retina travels to the cornea to interact with its receptor and trigger lens regeneration. The described experiments found that FGF1, FGF8, and FGF9 mRNA are more expressed in the retina than the cornea, indicating that they may be the signal for inducing lens regeneration. Three receptor mRNAs (FGFR1, FGFR2, and FGFR3) were found to be expressed in the cornea. Second, the necessity of FGFR signaling was investigated in vitro using a small molecule inhibitor (SU5402) and dominant negative FGFR1. Both experiments demonstrated that lens regeneration is inhibited upon FGFR signaling inhibition, indicating the necessity of FGFR signaling in lens regeneration. Finally, the sufficiency of various factors for lens regeneration was tested using an in vitro cornea culture assay. FGF1 strongly induced lens formation, and FGF8 also appeared to weakly induce lens formation, whereas FGF2 and FGF9 did not induce lens formation. In addition, insulin and FBS also appeared to induce lens formation in cornea cultures. Overall, this dissertation illuminates the roles that FGF signaling play in Xenopus laevis lens regeneration. In the future, this work may guide subsequent research in treating eye diseases.
Advisors/Committee Members: Henry, Jonathan J (advisor), Henry, Jonathan J. (Committee Chair), Chen, Jie (committee member), Newmark, Phillip A. (committee member), Raetzman, Lori T. (committee member), Smith-Bolton, Rachel (committee member).
Subjects/Keywords: Xenopus laevis; lens; cornea; regeneration; Fibroblast Growth Factors (FGF); Fibroblast Growth Factor Receptors (FGFR)
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Moore, L. (2015). FGF signaling in Xenopus laevis lens regeneration. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/78759
Chicago Manual of Style (16th Edition):
Moore, Lisa. “FGF signaling in Xenopus laevis lens regeneration.” 2015. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed April 18, 2021.
http://hdl.handle.net/2142/78759.
MLA Handbook (7th Edition):
Moore, Lisa. “FGF signaling in Xenopus laevis lens regeneration.” 2015. Web. 18 Apr 2021.
Vancouver:
Moore L. FGF signaling in Xenopus laevis lens regeneration. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2015. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2142/78759.
Council of Science Editors:
Moore L. FGF signaling in Xenopus laevis lens regeneration. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2015. Available from: http://hdl.handle.net/2142/78759

Queen Mary, University of London
8.
Mistry, J. N.
Defining the role of fibroblast growth factor 21 (FGF21) in the pathogenesis of growth hormone resistance and subsequent growth failure in chronic childhood conditions.
Degree: PhD, 2019, Queen Mary, University of London
URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/55457
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786344
► Fibroblast growth factor 21 (FGF21) is an essential metabolic regulator, adapting to changes in nutritional status. Excessive undernutrition is suggested to elevate FGF21 levels, developing…
(more)
▼ Fibroblast growth factor 21 (FGF21) is an essential metabolic regulator, adapting to changes in nutritional status. Excessive undernutrition is suggested to elevate FGF21 levels, developing Growth hormone (GH) resistance and subsequent linear growth attenuation through unknown mechanisms. The aim of this PhD was to unravel in vitro the mechanistic interplay of FGF21 on GH receptor (GHR) signalling, further determining the association between nutrition induced chronic FGF21 using postnatal growth failure of very pre-term (VPT) infants as a model. FGF21 and receptor complex (FGFR1/-IIIC/β-Klotho) expression was evaluated in newly established HEK-293 stably expressing human/ mouse GHR. Human growth plate tissue was examined for the localisation of FGF21 and co-receptors within growth plate zonation. Cell lines and/or human growth plate explants were tested for GHR half-life and key GHR signalling mediators; STAT5, SOCS2 and IGF-1 in the presence/ absence of recombinant GH and FGF21. Serially measured FGF21/ IGF-1 levels and nutritional intake were assessed for the association with linear growth trends in VPT infants. The molecular integrity of GHR signalling and expression of FGF21 and receptors; FGFR1/-IIIC/β-KLOTHO was confirmed in stable lines. FGF21 and co-receptors were localised within the proliferative and pre-hypertrophic zones of human growth plate tissue. FGF21 increased GH-induced GHR turnover and SOCS2 expression; leading to the inhibition of downstream GHR signalling events including; pSTAT5 and IGF-1 expression. VPT infants displayed an immediate growth failure after birth followed by catch-up. FGF21 levels were elevated during growth deflection compared to catch-up (p < 0.001). A positive association of fat (β=8.83, p=0.004) and carbohydrate (β=4.11, p=0.006) intake after birth was associated with the change in SD score for length catch-up growth. Chronic FGF21 inhibited GHR signalling events, playing a central role in GH resistance and growth failure. Nutrition did not regulate hormonal levels, having a direct effect on linear growth catch-up in VPT infants.
Subjects/Keywords: Fibroblast growth factor 21; FGF21; postnatal growth failure
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APA (6th Edition):
Mistry, J. N. (2019). Defining the role of fibroblast growth factor 21 (FGF21) in the pathogenesis of growth hormone resistance and subsequent growth failure in chronic childhood conditions. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/55457 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786344
Chicago Manual of Style (16th Edition):
Mistry, J N. “Defining the role of fibroblast growth factor 21 (FGF21) in the pathogenesis of growth hormone resistance and subsequent growth failure in chronic childhood conditions.” 2019. Doctoral Dissertation, Queen Mary, University of London. Accessed April 18, 2021.
http://qmro.qmul.ac.uk/xmlui/handle/123456789/55457 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786344.
MLA Handbook (7th Edition):
Mistry, J N. “Defining the role of fibroblast growth factor 21 (FGF21) in the pathogenesis of growth hormone resistance and subsequent growth failure in chronic childhood conditions.” 2019. Web. 18 Apr 2021.
Vancouver:
Mistry JN. Defining the role of fibroblast growth factor 21 (FGF21) in the pathogenesis of growth hormone resistance and subsequent growth failure in chronic childhood conditions. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2019. [cited 2021 Apr 18].
Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/55457 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786344.
Council of Science Editors:
Mistry JN. Defining the role of fibroblast growth factor 21 (FGF21) in the pathogenesis of growth hormone resistance and subsequent growth failure in chronic childhood conditions. [Doctoral Dissertation]. Queen Mary, University of London; 2019. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/55457 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786344
9.
Pauley, Sarah.
Fibroblast Growth Factor Expression in Inner Correlates with Defects in the Null Mutant.
Degree: M.S. in Biomedical Sciences, Biomedical Sciences (graduate program), 2001, Creighton University
URL: http://hdl.handle.net/10504/65393
► The inner ear is a multifunctional organ required for hearing, balance, and proprioception of the head. Each area of sensory cells in the ear must…
(more)
▼ The inner ear is a multifunctional organ required for hearing, balance, and proprioception of the head. Each area of sensory cells in the ear must develop to be perfectly situated to receive specific stimulation. Formally, the development of the inner ear can be divided into three components: cell fate assignment, morphogenesis, and proliferation. Cell fate assignment is highly conserved throughout evolution and the same genes are utilized for this task both in mice and insects. In contrast, morphogenesis is poorly conserved evolutionarily, utilizing unique genes or unique gene combinations in higher organisms.|The insect gene corresponding to the
fibroblast growth factors (FGFs) does not appear in insect mechanosensor development. However, several of the greatly expanded, 24 member, mammalian FGF family of genes are expressed during the development of the inner ear. Therefore, these genes are considered to appear late in the evolution of the ear and expected to participate in morphogenesis.|FGFs are crucial for branching of the limbs and lungs in mice. Expression patterns in the development of these structures can be used as a model for expression in the ear since many of the same genes are utilized in both budding morphogenesis and ear formation.|The expression pattern of FGF3, 8, 9, and 10 were analyzed in the inner ear. FGF10 has a very stable expression pattern in the sensory epithelia, particularly in the canals, and in the VIIIth ganglion. From this data, FGF10 involvement is expected in the development of the canals and sensory epithelia but its specific activities cannot be determined by expression pattern alone.|Amgen produced mice that do not express FGF10, and they reported the lack of limbs and lungs in these FGF10 null mutants. This lack of budding morphogenesis makes .it impossible to evaluate the loss of gene expression on these structures. However, the mutants do form ears and the malformations in theses ears can be correlated with the FGF10 expression in the normal ear. In the inner ear of the FGF10 null mutants the canals are truncated and the orientation of the canals and the sensory epithelia are dramatically altered. Furthermore, the posterior vertical canal appears to be missing entirely. These data, in addition to FGF10 expression data, imply that E'GFIO is critical for defining polarity of the inner ear on both a global and local scale.
Advisors/Committee Members: Fritzsch, Bernd (advisor), Pauley, Sarah (cuauthor).
Subjects/Keywords: Fibroblast Growth Factor 2; Receptors, Fibroblast Growth Factor – genetics
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Pauley, S. (2001). Fibroblast Growth Factor Expression in Inner Correlates with Defects in the Null Mutant. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/65393
Chicago Manual of Style (16th Edition):
Pauley, Sarah. “Fibroblast Growth Factor Expression in Inner Correlates with Defects in the Null Mutant.” 2001. Masters Thesis, Creighton University. Accessed April 18, 2021.
http://hdl.handle.net/10504/65393.
MLA Handbook (7th Edition):
Pauley, Sarah. “Fibroblast Growth Factor Expression in Inner Correlates with Defects in the Null Mutant.” 2001. Web. 18 Apr 2021.
Vancouver:
Pauley S. Fibroblast Growth Factor Expression in Inner Correlates with Defects in the Null Mutant. [Internet] [Masters thesis]. Creighton University; 2001. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/10504/65393.
Council of Science Editors:
Pauley S. Fibroblast Growth Factor Expression in Inner Correlates with Defects in the Null Mutant. [Masters Thesis]. Creighton University; 2001. Available from: http://hdl.handle.net/10504/65393
10.
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki.
Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.
Degree: 博士(歯学), 2014, Fukuoka Dental College / 福岡歯科大学
URL: http://id.nii.ac.jp/1167/00000003/
► Transforming growth factor-β1 (TGF-β1) reportedly causes the differentiation of fibroblasts to myofibroblasts during wound healing. We investigated the mechanism underlying the activation of latent TGF-β1…
(more)
▼ Transforming growth factor-β1 (TGF-β1) reportedly causes the differentiation of fibroblasts to myofibroblasts during wound healing. We investigated the mechanism underlying the activation of latent TGF-β1 released by keratinocytes in efforts to identify promising pharmacological approaches for the prevention of hypertrophic scar formation. A three-dimensional collagen gel matrix culture was prepared using rat keratinocytes and dermal fibroblasts. Stratified keratinocytes promoted the TGF receptor-dependent increase in α-smooth muscle actin (α-SMA) immunostaining and mRNA levels in fibroblasts. Latent TGF-β1 was found to be localized suprabasally and secreted. α-SMA expression was inhibited by an anti-αv-integrin antibody and a matrix metalloproteinase (MMP) inhibitor, GM6001. In a two-dimensional fibroblast culture, α-SMA expression depended on the production of endogenous TGF-β1 and required αv-integrin or MMP for the response to recombinant latent TGF-β1. In keratinocyte-conditioned medium, MMP-dependent latent TGF-β1 secretion was detected. Applying this medium to the fibroblast culture enhanced α-SMA production. This effect was decreased by GM6001, the anti-αv-integrin antibody, or the preabsorption of latent TGF-β1. These results indicate that keratinocytes secrete latent TGF-β1, which is liberated to fibroblasts over distance and is activated to produce α-SMA with the aid of a positive-feedback loop. MMP inhibition was effective for targeting both keratinocytes and fibroblasts in this model.
2013年度
Subjects/Keywords: keratinocyte; fibroblast; transforming growth factor-β1; αv-integrin; matrix metalloproteinase
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, H. (2014). Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000003/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed April 18, 2021.
http://id.nii.ac.jp/1167/00000003/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Web. 18 Apr 2021.
Vancouver:
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. [cited 2021 Apr 18].
Available from: http://id.nii.ac.jp/1167/00000003/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. Available from: http://id.nii.ac.jp/1167/00000003/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
11.
小林, 信博.
Porous Alpha-Tricalcium Phosphate with Immobilized Basic Fibroblast Growth Factor Enhances Bone Regeneration in a Canine Mandibular Bone Defect Model : イヌ下顎骨骨欠損モデルにおいて塩基性線維芽細胞増殖因子を固定させたα-リン酸三カルシウム多孔質体は骨再生を促進させる.
Degree: 博士(歯学), 2017, Osaka Dental University / 大阪歯科大学
URL: http://id.nii.ac.jp/1392/00000138/
► The effect of porous alpha-tricalcium phosphate (-TCP) with immobilized basic fibroblast growth factor (bFGF) on bone regeneration was evaluated in a canine mandibular bone defect…
(more)
▼ The effect of porous alpha-tricalcium phosphate (-TCP) with immobilized basic fibroblast growth factor (bFGF) on bone regeneration was evaluated in a canine mandibular bone defect model. Identical bone defects were made in the canine mandible; six defects in each animal were filled with porous α-TCP with bFGF bound via heparin (bFGF group), whereas the other was filled with unmodified porous α-TCP (control group). Micro-computed tomography and histological evaluation were performed 2, 4, and 8 weeks after implantation. The bone mineral density of the bFGF group was higher than that of the control group at each time point (P < 0.05), and the bone mineral content of the bFGF group was higher than that of the control group at 4 and 8 weeks (P < 0.05). Histological evaluation 2 weeks after implantation revealed that the porous -TCP had degraded and bone had formed on the surface of -TCP particles in the bFGF group. At 8 weeks, continuous cortical bone with a Haversian structure covered the top of bone defects in the bFGF group. These findings demonstrate that porous -TCP with immobilized bFGF can promote bone regeneration.
2016年度
Subjects/Keywords: alpha-tricalcium phosphate |basic fibroblast growth factor | bone regeneration
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
小林, . (2017). Porous Alpha-Tricalcium Phosphate with Immobilized Basic Fibroblast Growth Factor Enhances Bone Regeneration in a Canine Mandibular Bone Defect Model : イヌ下顎骨骨欠損モデルにおいて塩基性線維芽細胞増殖因子を固定させたα-リン酸三カルシウム多孔質体は骨再生を促進させる. (Thesis). Osaka Dental University / 大阪歯科大学. Retrieved from http://id.nii.ac.jp/1392/00000138/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
小林, 信博. “Porous Alpha-Tricalcium Phosphate with Immobilized Basic Fibroblast Growth Factor Enhances Bone Regeneration in a Canine Mandibular Bone Defect Model : イヌ下顎骨骨欠損モデルにおいて塩基性線維芽細胞増殖因子を固定させたα-リン酸三カルシウム多孔質体は骨再生を促進させる.” 2017. Thesis, Osaka Dental University / 大阪歯科大学. Accessed April 18, 2021.
http://id.nii.ac.jp/1392/00000138/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
小林, 信博. “Porous Alpha-Tricalcium Phosphate with Immobilized Basic Fibroblast Growth Factor Enhances Bone Regeneration in a Canine Mandibular Bone Defect Model : イヌ下顎骨骨欠損モデルにおいて塩基性線維芽細胞増殖因子を固定させたα-リン酸三カルシウム多孔質体は骨再生を促進させる.” 2017. Web. 18 Apr 2021.
Vancouver:
小林 . Porous Alpha-Tricalcium Phosphate with Immobilized Basic Fibroblast Growth Factor Enhances Bone Regeneration in a Canine Mandibular Bone Defect Model : イヌ下顎骨骨欠損モデルにおいて塩基性線維芽細胞増殖因子を固定させたα-リン酸三カルシウム多孔質体は骨再生を促進させる. [Internet] [Thesis]. Osaka Dental University / 大阪歯科大学; 2017. [cited 2021 Apr 18].
Available from: http://id.nii.ac.jp/1392/00000138/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
小林 . Porous Alpha-Tricalcium Phosphate with Immobilized Basic Fibroblast Growth Factor Enhances Bone Regeneration in a Canine Mandibular Bone Defect Model : イヌ下顎骨骨欠損モデルにおいて塩基性線維芽細胞増殖因子を固定させたα-リン酸三カルシウム多孔質体は骨再生を促進させる. [Thesis]. Osaka Dental University / 大阪歯科大学; 2017. Available from: http://id.nii.ac.jp/1392/00000138/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University
12.
Girer, Nathaniel Gabriel.
AN EXAMINATION OF THE ARYL HYDROCARBON RECEPTOR IN LIVER METABOLISM.
Degree: 2016, Penn State University
URL: https://submit-etda.libraries.psu.edu/catalog/13610nug128
► The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor from the basic helix-loop-helix PER/ARNT/SIM family of proteins that is evolutionarily conserved in both vertebrates…
(more)
▼ The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription
factor from the basic helix-loop-helix PER/ARNT/SIM family of proteins that is evolutionarily conserved in both vertebrates and invertebrates. Known as a "promiscuous" receptor, AHR can bind to several different classes of chemical compounds such as polycyclic aromatic hydrocarbons (PAH) and flavonoids. When not bound to ligand, AHR resides in a cytosolic complex containing two molecules of heat shock protein 90, one molecule of X-associated protein 2, and a molecule of p23. Upon ligand binding, this complex is transported to the nucleus via nuclear importins and AHR dissociates to form a heterodimer with aryl hydrocarbon nuclear translocator (ARNT). The AHR/ARNT heterodimer then binds to specific DNA sequences known as dioxin response elements (DRE) within the promoter region of target genes (e.g. cytochrome P450 enzyme 1A1, CYP1A1) to activate their transcription.
Previous studies have primarily examined AHR within the context of ligand-mediated transcriptional activation of its prototypical target gene, Cyp1a1. However, the AHR can also influence gene transcription in the absence of exogenous ligand and/or Cyp1a1 expression. Using a conditional AHR knockout mouse model that lacks hepatocyte-specific AHR expression (Ahrfx/fxAlbCre), this dissertation examines how basal AHR activity in the absence of Cyp1a1 transcription can influence metabolic homeostasis. In particular, the data reveal that the loss of hepatocyte-specific AHR expression correlates with reduced body and liver mass relative to congenic AHR-expressing mice (Ahrfx/fx). Additionally, Ahrfx/fxAlbCre mice maintained on purified AIN-93M diet display impaired glucose tolerance without any perturbations of insulin sensitivity. Conversely, Ahrfx/fxAlbCre mice challenged with a high-sucrose dietary modification of AIN-93M exhibit reduced insulin sensitivity without any difference in glucose tolerance. Most notably, Ahrfx/fxAlbCre mice challenged with a high-fat/high-sucrose (HF/HS) diet exhibit significantly decreased gene/protein expression of key enzymes involved in de novo fatty acid synthesis and fatty acid import, as well as significantly increased expression of key fatty acid export genes. Furthermore, inflammatory gene expression is also significantly reduced in HF/HS-fed Ahrfx/fxAlbCre mice relative to Ahrfx/fx. Together, the data suggest that basal hepatocyte-specific AHR signaling may promote diet-induced steatohepatitis in Ahrfx/fx mice.
Utilizing the Ahrfx/fxAlbCre mouse model, this dissertation also explores the role of AHR in regulating hepatic
fibroblast growth factor 21 (FGF21) production. FGF21 is an important metabolic hormone and regulator of the fasting response. Notably, FGF21 can attenuate obesity-associated morbidities when administered to various genetic and diet-induced mouse models of the disease. In the absence of exogenous AHR ligand, non-fasted Ahrfx/fxAlbCre mice exhibit 4-fold greater hepatic Fgf21 expression relative to Ahrfx/fx, along with elevated…
Advisors/Committee Members: Gary Perdew, Dissertation Advisor/Co-Advisor, Gary Perdew, Committee Chair/Co-Chair, Andrew Patterson, Committee Member, Jeffrey Peters, Committee Member, Connie Rogers, Outside Member, Ross Hardison, Committee Member, Ross Hardison, Committee Member.
Subjects/Keywords: Aryl Hydrocarbon Receptor; Fibroblast growth factor 21; Liver Metabolism
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Girer, N. G. (2016). AN EXAMINATION OF THE ARYL HYDROCARBON RECEPTOR IN LIVER METABOLISM. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/13610nug128
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Girer, Nathaniel Gabriel. “AN EXAMINATION OF THE ARYL HYDROCARBON RECEPTOR IN LIVER METABOLISM.” 2016. Thesis, Penn State University. Accessed April 18, 2021.
https://submit-etda.libraries.psu.edu/catalog/13610nug128.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Girer, Nathaniel Gabriel. “AN EXAMINATION OF THE ARYL HYDROCARBON RECEPTOR IN LIVER METABOLISM.” 2016. Web. 18 Apr 2021.
Vancouver:
Girer NG. AN EXAMINATION OF THE ARYL HYDROCARBON RECEPTOR IN LIVER METABOLISM. [Internet] [Thesis]. Penn State University; 2016. [cited 2021 Apr 18].
Available from: https://submit-etda.libraries.psu.edu/catalog/13610nug128.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Girer NG. AN EXAMINATION OF THE ARYL HYDROCARBON RECEPTOR IN LIVER METABOLISM. [Thesis]. Penn State University; 2016. Available from: https://submit-etda.libraries.psu.edu/catalog/13610nug128
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University
13.
Huang, Yanqing.
Fibroblast Growth Factor Signaling in Prostate Stem Cells and Prostate Cancer.
Degree: PhD, Biomedical Sciences, 2015, Texas A&M University
URL: http://hdl.handle.net/1969.1/155497
► The prostate is an androgen-dependent male reproductive organ that is comprised of epithelial and stromal compartments. The epithelial compartment contains basal, luminal, and neuroendocrine cells.…
(more)
▼ The prostate is an androgen-dependent male reproductive organ that is comprised of epithelial and stromal compartments. The epithelial compartment contains basal, luminal, and neuroendocrine cells. Two types of prostate epithelial stem cells (P-SCs), basal stem cells and luminal stem cells, have been identified in both human and mouse adult prostates based on tissue recombination models, cell lineage tracing, and in vitro prostasphere or organoid cultures. Using lineage-tracing with P63CreERT2 and prostasphere culture, we show here that the sphere-forming P-SCs are P63-expressing cells and reside in the basal compartment. Therefore we designate them as basal P-SCs (P-bSCs). P-bSCs are capable of differentiating into AR+ and CK18+ organoid cells, but not vice versa. We also report that prostaspheres contain quiescent stem cells, which possess more potent self-renewal capacity. Distinct from other tissue stem cells, P-bSCs do not contain Lgr5+ cells.
The
fibroblast growth factor signaling axis regulates embryonic stem cell development as well as tissue specific stem cell maintenance and differentiation. However, the role of FGF signaling in P-SC self-renewal and differentiation is still elusive. We show that the type 2 FGF receptor (FGFR2) signaling axis is crucial for preserving self-renewal and preventing the differentiation of P-bSCs. FGFR2 signaling mediated by FGFR substrate 2α (FRS2α) is indispensable for formation and maintenance of prostaspheres derived from P63+ P-bSCs. Ablation of Fgfr2 in vivo reduces P63-expressing basal cells, and promotes basal-to-luminal differentiation. In addition, ablation of Fgfr2 in P63+ cells disrupts postnatal development of the prostate.
Accumulating evidence has also shown that prostate cancer (PCa) progression is frequently associated with dysregulation of FGF signaling. Herein, we report that forced expression of FGF9 in prostate epithelial cells leads to high grade prostatic intraepithelial neoplasia (PIN). Overexpression of FGF9 in TRAMP mice induces more malignant PCa and higher frequency of metastasis. Hyperproliferative stromal cells are shown in the F9TG and F9TRAMP mouse prostates. Reactive stroma which upregulates TGF-β1, was observed in F9TG and F9TRAMP prostates. We also show that transcription
factor c-Jun is a mediator in the FGF9-TGFβ1 axis.
Collectively, our study provides new insights into prostate stem cells and prostate cancer. Upset of the intricate balance of FGF signaling in the prostate disrupts stem cell homeostastasis and prostate development, and initiates prostate tumorigenesis.
Advisors/Committee Members: Wang, Fen (advisor), McKeehan, Wallace L (advisor), Navone, Nora M (committee member), Rowley, David R (committee member), Ittmann, Michael M (committee member).
Subjects/Keywords: Fibroblast Growth Factor; Prostate Stem Cells; Prostate Cancer
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Huang, Y. (2015). Fibroblast Growth Factor Signaling in Prostate Stem Cells and Prostate Cancer. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155497
Chicago Manual of Style (16th Edition):
Huang, Yanqing. “Fibroblast Growth Factor Signaling in Prostate Stem Cells and Prostate Cancer.” 2015. Doctoral Dissertation, Texas A&M University. Accessed April 18, 2021.
http://hdl.handle.net/1969.1/155497.
MLA Handbook (7th Edition):
Huang, Yanqing. “Fibroblast Growth Factor Signaling in Prostate Stem Cells and Prostate Cancer.” 2015. Web. 18 Apr 2021.
Vancouver:
Huang Y. Fibroblast Growth Factor Signaling in Prostate Stem Cells and Prostate Cancer. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/1969.1/155497.
Council of Science Editors:
Huang Y. Fibroblast Growth Factor Signaling in Prostate Stem Cells and Prostate Cancer. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155497

University of Texas Southwestern Medical Center
14.
Paulson, Vera Ashley.
High-Resolution Array Comparative Genomic Hybridization Identifies Common Targets in Rhabdomyosarcoma.
Degree: 2012, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/1112
► Rhabdomyosarcoma (RMS) accounts for nearly 50 percent of the soft tissue sarcomas that affect children. There are two major histological variants, alveolar (ARMS) and embryonal…
(more)
▼ Rhabdomyosarcoma (RMS) accounts for nearly 50 percent of the soft tissue sarcomas that affect children. There are two major histological variants, alveolar (ARMS) and embryonal (ERMS). Both are defined as sarcomas that show exclusive evidence of muscle differentiation, but differ in their pathogenesis and prognosis. ARMS typically occurs in adolescents, presents as disease of the extremities, has a higher risk of metastasis or treatment-resistance, and in 75% of cases, is characterized by the presence of the PAX3/7:FOXO1A translocation. ERMS is associated with a younger age at presentation, sites of disease other than the extremities, a more favorable clinical outcome, and the absence of consistent chromosomal translocations. Here we used high-density array-based comparative genomic hybridization to examine the genomes of RMS to identify common programs that drive tumor pathogenesis.
Advisors/Committee Members: Cameron, Scott.
Subjects/Keywords: Rhabdomyosarcoma; Gene Expression Regulation, Neoplastic; Receptor, Fibroblast Growth Factor, Type 4
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Paulson, V. A. (2012). High-Resolution Array Comparative Genomic Hybridization Identifies Common Targets in Rhabdomyosarcoma. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1112
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Paulson, Vera Ashley. “High-Resolution Array Comparative Genomic Hybridization Identifies Common Targets in Rhabdomyosarcoma.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed April 18, 2021.
http://hdl.handle.net/2152.5/1112.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Paulson, Vera Ashley. “High-Resolution Array Comparative Genomic Hybridization Identifies Common Targets in Rhabdomyosarcoma.” 2012. Web. 18 Apr 2021.
Vancouver:
Paulson VA. High-Resolution Array Comparative Genomic Hybridization Identifies Common Targets in Rhabdomyosarcoma. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2152.5/1112.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Paulson VA. High-Resolution Array Comparative Genomic Hybridization Identifies Common Targets in Rhabdomyosarcoma. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1112
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto
15.
Wei, Wangzhi.
The Role of Alternatively spliced Fibroblast Growth Factor Receptor 2 Isoforms in Breast Cancer.
Degree: 2011, University of Toronto
URL: http://hdl.handle.net/1807/31636
► Recent genome-wide association studies identified FGFR2 as one of breast cancer susceptibility genes. FGFR2 expression was down-regulated in breast carcinomas when compared with paired normal…
(more)
▼ Recent genome-wide association studies identified FGFR2 as one of breast cancer susceptibility genes. FGFR2 expression was down-regulated in breast carcinomas when compared with paired normal epithelium. Stable retroviral transduction of FGFR2-IIIb and its alternatively spliced FGFR2-IIIc variants was achieved in breast cancer MDA-MB-231, T47D and near normal MCF-10A cells. Our findings revealed a direct reduction of breast cancer cell growth and motility, a significant arrest of transformed morphogenetic changes including the Epithelial to Mesenchymal transition (EMT), anchorage independent growth, and the formation of growth-arrested 3D acinar architectures, and suppressive actions on orthotopically xenografted epithelial neoplasms and surrounding tumor stroma. These tumor protective effects were concordant with physical interactions between the two FGFR2 isoforms and IKKβ. Consistent with these interactions we noted FGFR2 to inhibit NF-κB signaling, including decreased nuclear RelA/p65 NF-κB localization, down-regulation of a transfected NF-κB luciferase reporter, reduced production of NF-κB-dependent transcripts, Interleukin-6 and p-STAT3.
MAST
Advisors/Committee Members: Ezzat, Shereen, Medical Science.
Subjects/Keywords: Fibroblast Growth Factor Receptor 2; Breast Cancer; NF-κB; 0992
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wei, W. (2011). The Role of Alternatively spliced Fibroblast Growth Factor Receptor 2 Isoforms in Breast Cancer. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/31636
Chicago Manual of Style (16th Edition):
Wei, Wangzhi. “The Role of Alternatively spliced Fibroblast Growth Factor Receptor 2 Isoforms in Breast Cancer.” 2011. Masters Thesis, University of Toronto. Accessed April 18, 2021.
http://hdl.handle.net/1807/31636.
MLA Handbook (7th Edition):
Wei, Wangzhi. “The Role of Alternatively spliced Fibroblast Growth Factor Receptor 2 Isoforms in Breast Cancer.” 2011. Web. 18 Apr 2021.
Vancouver:
Wei W. The Role of Alternatively spliced Fibroblast Growth Factor Receptor 2 Isoforms in Breast Cancer. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/1807/31636.
Council of Science Editors:
Wei W. The Role of Alternatively spliced Fibroblast Growth Factor Receptor 2 Isoforms in Breast Cancer. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/31636

University of Texas Southwestern Medical Center
16.
Boney-Montoya, Jamie.
Understanding the Molecular Basis for FGF15/19 and FGF21 Actions on Energy Homeostasis.
Degree: 2012, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/986
► Insulin and glucagon have long been known to play essential roles in controlling energy balance during the fed and fasted states, respectively. Recently, additional metabolic…
(more)
▼ Insulin and glucagon have long been known to play essential roles in controlling energy balance during the fed and fasted states, respectively. Recently, additional metabolic hormones have been discovered within a subfamily of the
fibroblast growth factor superfamily. The FGF15/19 subfamily is composed of atypical FGFs lacking the heparin-binding domain, which enables them to act in an endocrine fashion by diffusing away from their tissues of origin. They signal through cell-surface receptors complexed with β-Klotho, a membrane-spanning protein, to mediate signaling cascades that lead to physiological responses. One member, FGF19, causes reduced glucose and insulin levels with enhanced insulin sensitivity when expressed in transgenic mice. Another member, FGF21, has been shown to act as an insulin sensitizer pharmacologically by improving glucose tolerance and reducing insulin. The prevalence of metabolic disorders (e.g. type 2 diabetes) in today’s society has led to the investigation of these two endocrine FGFs for use in a clinical setting. However, the mechanisms underlying these responses have not been characterized.
To elucidate the mechanisms utilized by FGF15/19, we used several animal models to show a role for FGF15/19 in regulating hepatic glucose production. Like insulin, FGF15/19 represses gluconeogenesis. Specifically, FGF15/19 inhibits expression of the transcriptional coactivator PGC1α, a key regulator of gluconeogenic gene expression. The repressive effect of FGF15/19 on gluconeogenic gene expression is lost when PGC1α is overexpressed. FGF15/19 causes the dephosphorylation and inactivation of the transcription
factor CREB, thereby blunting its ability to bind and induce the PGC1α promoter. The results demonstrated that FGF15/19 works subsequent to insulin as a postprandial regulator of gluconeogenesis through inhibition of the CREB/ PGC1α pathway.
To fully understand the effects of FGF21, we began studying the downstream kinase signaling cascades and the protein substrates affected by this hormone. Utilizing stable isotope labeling of amino acids in cell culture (SILAC), an unbiased phosphoproteomic profile was obtained of potential FGF21 targets in rat H4IIE hepatoma cells. One of the most highly regulated targets was FetuinA, which was dephosphorylated by FGF21 treatment. FetuinA is an inhibitor of insulin receptor signaling and the FetuinA knockout mouse exhibits aberrant glucose homeostatsis. Our in vitro data suggested a relationship between FGF21 and FetuinA in regulating insulin sensitivity but further exploration lead to the conclusion that FGF21 was not directly regulating FetuinA in vivo.
Taken together, the important role of FGF15/19 and FGF21 in regulating carbohydrate metabolism as well as their pharmacological actions makes them attractive drug candidates for metabolic diseases. However, further study will be required to determine their molecular mechanisms more completely and their long-term efficacy in the clinic.
Advisors/Committee Members: Kliewer, Steven A..
Subjects/Keywords: Fibroblast Growth Factor; Glucose; Cyclic AMP Response Element-Binding Protein
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Boney-Montoya, J. (2012). Understanding the Molecular Basis for FGF15/19 and FGF21 Actions on Energy Homeostasis. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/986
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Boney-Montoya, Jamie. “Understanding the Molecular Basis for FGF15/19 and FGF21 Actions on Energy Homeostasis.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed April 18, 2021.
http://hdl.handle.net/2152.5/986.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Boney-Montoya, Jamie. “Understanding the Molecular Basis for FGF15/19 and FGF21 Actions on Energy Homeostasis.” 2012. Web. 18 Apr 2021.
Vancouver:
Boney-Montoya J. Understanding the Molecular Basis for FGF15/19 and FGF21 Actions on Energy Homeostasis. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2152.5/986.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Boney-Montoya J. Understanding the Molecular Basis for FGF15/19 and FGF21 Actions on Energy Homeostasis. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/986
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center
17.
Dutchak, Paul Anthony.
Metabolic Regulation by Fibroblast Growth Factor 21.
Degree: 2011, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/935
► Fibroblast growth factor 21 (FGF21) is a secreted hormone that can beneficially regulate glucose and lipid homeostasis. Through a reverse endocrinology approach, we uncovered that…
(more)
▼ Fibroblast growth factor 21 (FGF21) is a secreted hormone that can beneficially regulate glucose and lipid homeostasis. Through a reverse endocrinology approach, we uncovered that FGF21 expression is transcriptionally regulated by the peroxisome proliferator activated-receptor alpha (PPARa) in liver. PPARa is a member of the nuclear hormone receptor superfamily that is physiologically activated by increased fatty acid mobilization to liver during fasting, and regulates the genetic program whereby lipids are converted to ketone bodies through a process known as ketogenesis. Here, I show the effects of FGF21 as a fasting hormone that is expressed in liver and contributes to the regulation of adipose tissue and hepatic ketogenesis during the fasted state. Using in vitro and in vivo methods to investigate the effects of FGF21, a model whereby FGF21 stimulates lipolysis in adipose tissue was generated. Intriguingly, using our FGF21 transgenic mice, I observed the expression of many genes involved in lipogenesis was highly induced in adipose tissue in an FGF21-dependent manner. Moreover, many of these lipogenic genes were found to be down-regulated in adipose of the FGF21 knockout mouse. The inhibition of lipogenic genes in adipose tissue was associated with increased SUMOylation of PPARg protein in this tissue. Using a feeding-fasting paradigm, I found that FGF21 expression in the liver and adipose tissue was rhythmic, peaking in liver prior to feeding and peaking in the adipose after feeding. Furthermore, the induction of FGF21 by PPARg ligands suggested a unique function for this protein in adipose, independent from its role in the fasted state. To assess the contribution of FGF21 to the anti-diabetic properties of PPARg agonists (ie. thiazolidinediones), diet-induced obese wild type and Fgf21-/- mice were treated with the TZD rosiglitazone. Rosiglitazone produced a significant increase in adipose FGF21 expression, but decreased hepatic FGF21 mRNA and circulating FGF21 protein. These data suggest that FGF21 functions as an autocrine
factor within adipose tissue. Moreover, the therapeutic effects of rosiglitazone as an insulin sensitizer were lost in the Fgf21-/- mouse, as assessed by glucose and insulin tolerance tests. Several other effects of rosiglitazone were lost in the Fgf21-/- mice, including increased adipose mass, edema, and PPARg target gene expression in the adipose. These data indicated that PPARg can control the expression of FGF21, which functions as a feed-forward mechanism to stimulate PPARg target genes and PPARg dependent physiology. Since PPARg can be modified by SUMO on two different sites on the protein, in vitro experiments were performed to show that PPARg is SUMOylated at Lysine-107, a previously identified negative regulator of its transcriptional activity. Importantly, I found that treatment of Fgf21-/- adipocytes with FGF21 reduced the amount of SUMOylated PPARg, thereby allowing it to be it an active state. Collectively, these data reveal that FGF21 has two independent…
Advisors/Committee Members: Kliewer, Steven A..
Subjects/Keywords: Fibroblast Growth Factor; Liver; Peroxisome Proliferator-Activated Receptors
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Dutchak, P. A. (2011). Metabolic Regulation by Fibroblast Growth Factor 21. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/935
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Dutchak, Paul Anthony. “Metabolic Regulation by Fibroblast Growth Factor 21.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed April 18, 2021.
http://hdl.handle.net/2152.5/935.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Dutchak, Paul Anthony. “Metabolic Regulation by Fibroblast Growth Factor 21.” 2011. Web. 18 Apr 2021.
Vancouver:
Dutchak PA. Metabolic Regulation by Fibroblast Growth Factor 21. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2152.5/935.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Dutchak PA. Metabolic Regulation by Fibroblast Growth Factor 21. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/935
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University College London (University of London)
18.
Britto, Jonathan Anthony.
Syndromic craniofacial dysostosis : from genotype to phenotype : studies of FGFR gene expression in human craniofacial development and craniosynostosis.
Degree: PhD, 2001, University College London (University of London)
URL: https://discovery.ucl.ac.uk/id/eprint/10100497/
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268446
► Fibroblast growth factor receptors (FGFRs) are a subset of receptor tyrosine kinases. Receptor diversity results from the differential splicing of mRNA to generate membrane bound…
(more)
▼ Fibroblast growth factor receptors (FGFRs) are a subset of receptor tyrosine kinases. Receptor diversity results from the differential splicing of mRNA to generate membrane bound and secreted proteins. FGFRl, 2, and 3 signalling pathways appear fundamental to human skeletogenesis; as illustrated by a range of cranioskeletal and dwarfing dysplasias that occur as a result of activating FGFR mutations. These phenotypes include the syndromic craniofacial dysostoses, which are related human developmental disorders combining variable craniofacial anomaly with extracranial manifestations. Common to these syndromes is craniosynostosis, in which the fibrous cranial suture is prematurely replaced by bone. Mutations in FGFR3 additionally cause the dwarfing chondrodysplasias, which may also feature craniosynostosis and basicranial dysplasia. Analysis of the expression of FGFR 1-3, and the ligands FGF2, FGF4, and FGF7, has been undertaken in human craniofacial tissues representing early foetal, late foetal, and infant stages of development. All tissue was collected and studied within strict ethical guidelines. FGFR transcripts were detected using isoform specific probes in - situ hybridisation studies, whilst protein products were detected by immuno - histochemistry. FGFRl, 2, and 3 are differentially expressed throughout human cranioskeletal development and human craniosynostosis. In infant sagittal suture fusion, FGFRl is a marker of pre-osseous proliferative and early osseous differentiative stages, whereas the FGFR2 - Iglllc (BEK) isoform is a marker of later osseous differentiation. Differential expression of FGFR1-3 in human craniofacial development and infant craniosynostosis correlates with the clinical craniofacial dysmorphism of the related syndromes. Comparison of mutant FGFR2 - C278F and mFGFR2 - P253R human embryo-foetal cranial skeletogenesis to age - matched wild - type, suggests that FGFR2 functional gain results in negative - autoregulation of FGFR2 expression in- situ. Furthermore, the isoform - specific expression of FGFR2 and ligands in human palatogenesis predicts a dominant - negative role for FGFR2 - Igllla/b (KGFR) in the pathogenesis of Apert cleft palate.
Subjects/Keywords: 612; Fibroblast growth factor receptors
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Britto, J. A. (2001). Syndromic craniofacial dysostosis : from genotype to phenotype : studies of FGFR gene expression in human craniofacial development and craniosynostosis. (Doctoral Dissertation). University College London (University of London). Retrieved from https://discovery.ucl.ac.uk/id/eprint/10100497/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268446
Chicago Manual of Style (16th Edition):
Britto, Jonathan Anthony. “Syndromic craniofacial dysostosis : from genotype to phenotype : studies of FGFR gene expression in human craniofacial development and craniosynostosis.” 2001. Doctoral Dissertation, University College London (University of London). Accessed April 18, 2021.
https://discovery.ucl.ac.uk/id/eprint/10100497/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268446.
MLA Handbook (7th Edition):
Britto, Jonathan Anthony. “Syndromic craniofacial dysostosis : from genotype to phenotype : studies of FGFR gene expression in human craniofacial development and craniosynostosis.” 2001. Web. 18 Apr 2021.
Vancouver:
Britto JA. Syndromic craniofacial dysostosis : from genotype to phenotype : studies of FGFR gene expression in human craniofacial development and craniosynostosis. [Internet] [Doctoral dissertation]. University College London (University of London); 2001. [cited 2021 Apr 18].
Available from: https://discovery.ucl.ac.uk/id/eprint/10100497/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268446.
Council of Science Editors:
Britto JA. Syndromic craniofacial dysostosis : from genotype to phenotype : studies of FGFR gene expression in human craniofacial development and craniosynostosis. [Doctoral Dissertation]. University College London (University of London); 2001. Available from: https://discovery.ucl.ac.uk/id/eprint/10100497/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268446

University of Colorado
19.
Brooks, Leah Rae.
Fibroblast growth factor signaling in the developing serotonergic system and anxiety-related behavior.
Degree: PhD, Integrative Physiology, 2014, University of Colorado
URL: https://scholar.colorado.edu/iphy_gradetds/30
► Anxiety disorders are some of the most commonly diagnosed psychopathologies in both pediatric and adult populations and have been linked to disrupted brain serotonergic…
(more)
▼ Anxiety disorders are some of the most commonly diagnosed psychopathologies in both pediatric and adult populations and have been linked to disrupted brain serotonergic systems. The risk for adult anxiety disorders increases in people with a history of childhood or adolescent anxiety, and the average age of onset for anxiety is eleven years old. These data suggest that anxiety has neurodevelopmental origins, yet our understanding of how anxiety-related serotonergic neurocircuits are formed and how their malformation contributes to the etiology of anxiety disorders is far from complete. This dissertation examined the role of
fibroblast growth factor 8 (Fgf8) signaling in the development of midbrain serotonergic neurons and anxiety-like behavior. Fgf8 is a signaling molecule that coordinates the genesis of the putative midbrain region. My hypothesis is that moderately reduced Fgf8 signaling during development impacts the structure and function of anxiety-related serotonergic neuronal subpopulations, thereby leading to anxiety-related behavior. Using adult male mice genetically altered to produce one-third less Fgf8, we observed defects specifically in anxiety- and panic-related serotonergic subpopulations. These defects included 1) fewer serotonergic neurons, 2) abnormal activation and functional responses of serotonergic neurons following a stressful stimulus, and 3) increased baseline anxiety-like behaviors. The results from this dissertation expand our knowledge on how developmental disruption of specific subpopulations of serotonergic neurons can affect their structural and functional integrity, thereby contributing to the persistent manifestation of anxiety behaviors. Overall, this dissertation suggests a role of Fgf signaling in the neurodevelopment of circuits that are disrupted in anxiety and affective disorders.
Advisors/Committee Members: Pei-San Tsai, Christopher Lowry, Sondra Bland, Benjamin Greenwood, Robert Spencer.
Subjects/Keywords: Anxiety; Dorsal raphe; Fibroblast growth factor; Serotonin; Neuroscience and Neurobiology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Brooks, L. R. (2014). Fibroblast growth factor signaling in the developing serotonergic system and anxiety-related behavior. (Doctoral Dissertation). University of Colorado. Retrieved from https://scholar.colorado.edu/iphy_gradetds/30
Chicago Manual of Style (16th Edition):
Brooks, Leah Rae. “Fibroblast growth factor signaling in the developing serotonergic system and anxiety-related behavior.” 2014. Doctoral Dissertation, University of Colorado. Accessed April 18, 2021.
https://scholar.colorado.edu/iphy_gradetds/30.
MLA Handbook (7th Edition):
Brooks, Leah Rae. “Fibroblast growth factor signaling in the developing serotonergic system and anxiety-related behavior.” 2014. Web. 18 Apr 2021.
Vancouver:
Brooks LR. Fibroblast growth factor signaling in the developing serotonergic system and anxiety-related behavior. [Internet] [Doctoral dissertation]. University of Colorado; 2014. [cited 2021 Apr 18].
Available from: https://scholar.colorado.edu/iphy_gradetds/30.
Council of Science Editors:
Brooks LR. Fibroblast growth factor signaling in the developing serotonergic system and anxiety-related behavior. [Doctoral Dissertation]. University of Colorado; 2014. Available from: https://scholar.colorado.edu/iphy_gradetds/30

University of Manitoba
20.
Wang, Jie.
Fibroblast growth factor-16 and acute doxorubicin cardiotoxicity: a target for early protection.
Degree: Physiology and Pathophysiology, 2018, University of Manitoba
URL: http://hdl.handle.net/1993/33048
► Background: Doxorubicin is an anti-cancer drug that is widely used in chemotherapy. However, doxorubicin-induced cardiotoxicity is a major risk factor for cancer patients and survivors,…
(more)
▼ Background: Doxorubicin is an anti-cancer drug that is widely used in chemotherapy. However, doxorubicin-induced cardiotoxicity is a major risk
factor for cancer patients and survivors, and can lead to heart failure. Dexrazoxane is the only approved drug to offer protection against doxorubicin-induced cardiotoxicity, but its use is limited. Strategies are needed to protect the heart against doxorubicin-induced cardiotoxicity and still allow its effective treatment of cancer.
Fibroblast growth factors (FGFs) are a family of 23 multifunctional proteins, with properties that include effects on cell
growth, survival, efflux transport, and cytoprotection. FGF-16 is the only member of the family that is produced preferentially by postnatal cardiac myocytes. Production of cardiac-specific proteins, including α-actin, troponin I, and myosin light chain 2, are often targeted negatively by doxorubicin due to effects at the transcriptional level. In addition, evidence including from FGF-16 null mice that were stressed through chronic high blood pressure, suggests FGF-16 contributes to the maintenance of a healthy myocardium and may have cardioprotective properties.
Hypothesis: FGF-16 synthesis (transcription) is an early target of doxorubicin, and decreased endogenous FGF-16 levels will decrease cardiac myocyte survival and, as a result, may contribute to a decreased resistance to heart damage. Thus, maintaining and/or increasing cardiac FGF-16 levels will increase resistance to doxorubicin-induced cardiotoxicity. This is due, at least in part, to a specific effect on efflux drug transport consistent with a decrease in intracellular doxorubicin concentration in cardiac myocytes.
Approaches and Results: Using quantitative polymerase chain reaction, FGF-16 messenger RNA levels were significantly decreased within 6 hours of doxorubicin treatment in both 8-week-old rat hearts and neonatal rat cardiac myocytes. The latter was linked to decreased transcription
factor Csx/Nkx2.5 association with the FGF-16 gene promoter, based on the results of transient gene transfer, protein binding, and RNA stability assays. Together with the relatively short FGF-16 mRNA half-life (~1.75 hours), FGF-16 is an early target of doxorubicin-induced cardiotoxicity. Furthermore, a decrease in FGF-16 production using FGF-16 siRNA “knockdown” was linked to reduced cardiac myocyte survival, while an increase in FGF-16 levels using adenoviral delivery was associated with resistance to doxorubicin-induced cardiac dysfunction and cardiac myocyte death; the latter corresponded to an increase in efflux transport of calcein AM and doxorubicin.
Discussion: Observations made demonstrate that postnatal cardiac-specific FGF-16 synthesis is an early target of acute doxorubicin-induced cardiotoxicity due to a negative effect on the cardiac transcription
factor Csx/Nkx2.5 and the relatively unstable FGF-16 transcripts. Endogenous FGF-16 helps maintain neonatal cardiac myocyte viability, while exogenous FGF-16 is protective by, at least in part, upregulation of…
Advisors/Committee Members: Cattini, Peter A. (Physiology and Pathophysiology) (supervisor), Czubryt, Michael (Physiology and Pathophysiology) Nachtigal, Mark (Biochemistry and Medical Genetics) Kardami, Elissavet (Human Anatomy and Cell Science) Fernig, David (University of Liverpool) (examiningcommittee).
Subjects/Keywords: Fibroblast growth factor 16; doxorubicin; multidrug resistance protein 1; cardioprotection
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wang, J. (2018). Fibroblast growth factor-16 and acute doxorubicin cardiotoxicity: a target for early protection. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/33048
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Wang, Jie. “Fibroblast growth factor-16 and acute doxorubicin cardiotoxicity: a target for early protection.” 2018. Thesis, University of Manitoba. Accessed April 18, 2021.
http://hdl.handle.net/1993/33048.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wang, Jie. “Fibroblast growth factor-16 and acute doxorubicin cardiotoxicity: a target for early protection.” 2018. Web. 18 Apr 2021.
Vancouver:
Wang J. Fibroblast growth factor-16 and acute doxorubicin cardiotoxicity: a target for early protection. [Internet] [Thesis]. University of Manitoba; 2018. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/1993/33048.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wang J. Fibroblast growth factor-16 and acute doxorubicin cardiotoxicity: a target for early protection. [Thesis]. University of Manitoba; 2018. Available from: http://hdl.handle.net/1993/33048
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université Catholique de Louvain
21.
Vietti, Giulia.
Molecular and cellular mechanisms of the pro-fibrotic effects of carbon nanotubes.
Degree: 2016, Université Catholique de Louvain
URL: http://hdl.handle.net/2078.1/174071
► Carbon nanotubes (CNT) are molecular-scale tubes of graphene sheets rolled into cylinders with peculiar characteristics that make them highly attractive for numerous industrial applications. Thus,…
(more)
▼ Carbon nanotubes (CNT) are molecular-scale tubes of graphene sheets rolled into cylinders with peculiar characteristics that make them highly attractive for numerous industrial applications. Thus, investigating the health hazards of CNT is of great importance in view of the increased potential for human exposure within occupational, environmental, and consumer environments. Several studies have already shown that CNT can induce inflammatory, fibrotic or carcinogenic reactions in the lung of experimental animals. These toxic responses appear, however, determined by the physico-chemical characteristics of CNT. This work focuses on lung fibrosis, a process involving the proliferation and activation of fibroblasts. The main objectives were (1) to understand the mechanisms mediating the fibrogenic activity of CNT by investigating their direct and indirect (via macrophages and epithelial cells) effects on fibroblasts and (2) to develop valid in vitro models to predict the fibrogenic activity of CNT. An additional objective was to assess and to identify physico-chemical properties of CNT that determine their fibrogenic activity. As CNT have been shown to interact with several toxicological assays, we first designed an adapted protocol of the WST-1 cell viability assay to avoid or take into account interferences of nanomaterials. Our data demonstrate that the direct in vitro activity of CNT on fibroblast proliferation strongly reflects their fibrogenic activity in vivo, supporting a predictive value of this in vitro endpoint. Kinase receptors, ERK 1/2 signaling and endocytosis were identified as mechanisms involved in fibroblast proliferation induced by fibrogenic CNT. In addition, we showed that CNT indirectly stimulate fibroblast differentiation, via epithelial cells and macrophages, highlighting the contribution of these cells in the development of fibrosis. We found that the release of IL-6 from epithelial cells is another useful biomarker, in addition to the proliferative activity of CNT on fibroblasts, to predict the toxic potential of CNT. The results also confirm that the length and diameter of CNT constitute important physico-chemical determinants of their capacity to induce lung fibrosis. Finally, we have organized, analyzed and integrated all the current knowledge concerning the mechanisms of action of CNT relevant for their pro-fibrotic activity in a tentative adverse outcome pathway (AOP). This provides a global picture of the complex network of events contributing to the fibrogenic activity of CNT, and allows identifying predictive in vitro endpoints useful for the toxicological assessment of new and emerging CNT.
(BIFA - Sciences biomédicales et pharmaceutiques) – UCL, 2016
Advisors/Committee Members: UCL - SSS/IREC/LTAP - Louvain Centre for Toxicology and Applied Pharmacology, UCL - Faculté de pharmacie et des sciences biomédicales, Lison, Dominique, van den Brule, Sybille, Hoet, Peter, Demoulin, Jean-Baptiste, Poland, Craig, Lanone, Sophie, Preat, Véronique.
Subjects/Keywords: Proliferation; Lung fibrosis; Fibroblast; Carbon nanotube; Adverse outcome pathway; Growth factor
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Vietti, G. (2016). Molecular and cellular mechanisms of the pro-fibrotic effects of carbon nanotubes. (Thesis). Université Catholique de Louvain. Retrieved from http://hdl.handle.net/2078.1/174071
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Vietti, Giulia. “Molecular and cellular mechanisms of the pro-fibrotic effects of carbon nanotubes.” 2016. Thesis, Université Catholique de Louvain. Accessed April 18, 2021.
http://hdl.handle.net/2078.1/174071.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Vietti, Giulia. “Molecular and cellular mechanisms of the pro-fibrotic effects of carbon nanotubes.” 2016. Web. 18 Apr 2021.
Vancouver:
Vietti G. Molecular and cellular mechanisms of the pro-fibrotic effects of carbon nanotubes. [Internet] [Thesis]. Université Catholique de Louvain; 2016. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/2078.1/174071.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Vietti G. Molecular and cellular mechanisms of the pro-fibrotic effects of carbon nanotubes. [Thesis]. Université Catholique de Louvain; 2016. Available from: http://hdl.handle.net/2078.1/174071
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
22.
Tanner, Yasmine.
Drug resistance mechanisms of FGFR-driven cancers.
Degree: PhD, 2019, Queen Mary, University of London
URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/56803
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775329
► The fibroblast growth factor (FGF) signalling pathway contributes to the regulation of a variety of cellular functions, affecting differentiation, migration, proliferation, and survival. Unsurprisingly, cancer…
(more)
▼ The fibroblast growth factor (FGF) signalling pathway contributes to the regulation of a variety of cellular functions, affecting differentiation, migration, proliferation, and survival. Unsurprisingly, cancer cells can hijack this pathway for growth or survival advantages, through alterations in ligands, receptors or regulatory molecules. Sequencing consortia have highlighted how mutation, amplification, translocation or loss of elements in the FGF signalling network can contribute to tumourigenesis, and the pathway is a major clinical target. Many FGF receptor (FGFR) driven cancers develop resistance against commonly used receptor tyrosine kinase (RTK) targeted therapeutics and dissection of the mechanisms that underlie this, both in the cancer cell, and also via stromal crosstalk in the tumour microenvironment, is of utmost importance to the development of therapeutic approaches to treat FGFR-driven cancers. In this work, I focus on the mechanisms of FGF deregulation and the impact of stromal cells. I aim to identify the implications of FGFR2 aberrations on gastric and endometrial cancer, and FGFR1 aberrations on lung cancer. Furthermore, I aim to dissect the mechanisms by which targeted cells may develop drug resistance both in two-dimensional (2D) and in a more physiomimetic three-dimensional (3D) co-culture model. It was established that cancer cells with FGFR aberrations were sensitive towards FGFR inhibitors such as PD173074 (PD), AZD4547 (AZD) and BGJ398 (BGJ). Cancer cells could be killed with increasing concentration of these drugs and exhibited sensitivity to FGFR inhibitors by decreased p-AKT and p-ERK signalling. However, with prolonged exposure to FGFR inhibition, certain cells began to acquire resistance in 2D. To study drug resistance in a more physiomimetic environment, cells were grown alone or co-cultured with fibroblasts and treated with FGFR inhibitors PD, AZD or BGJ and imaged using fluorescent live cell imaging. These cultures were then fixed, paraffin embedded and immuno- or Haematoxylin and Eosin (H&E) stained. To study the emergence of drug resistance in 3D with and without stromal support, cells were seeded into Alvetex® scaffolds and treated with increasing concentrations of BGJ until resistant populations were observed via confocal fluorescence microscopy. Cancer cells grown in co-culture with fibroblasts acquired resistance faster than monoculture cells. Significantly regulated genes between resistant and parental mono- and co-culture cells were identified using ribonucleic acid sequencing (RNA-Seq) and bioinformatics. The majority of significantly regulated pathways in FGFR2-amplifed gastric cancer cells, were metabolic pathways including retinol metabolism, starch and sucrose degradation, which was mainly driven by sucrose-isomaltase (SI) and aldolase B (ALDOB), resulting in glucose generation. Targets were then modified using different approaches such as knockdown, overexpression and drug treatments to observe how this affects resistance of FGFR-driven cancers. Blockade of ALDOB…
Subjects/Keywords: fibroblast growth factor; cancer; drug resistance; FGFR-driven cancers
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Tanner, Y. (2019). Drug resistance mechanisms of FGFR-driven cancers. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/56803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775329
Chicago Manual of Style (16th Edition):
Tanner, Yasmine. “Drug resistance mechanisms of FGFR-driven cancers.” 2019. Doctoral Dissertation, Queen Mary, University of London. Accessed April 18, 2021.
http://qmro.qmul.ac.uk/xmlui/handle/123456789/56803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775329.
MLA Handbook (7th Edition):
Tanner, Yasmine. “Drug resistance mechanisms of FGFR-driven cancers.” 2019. Web. 18 Apr 2021.
Vancouver:
Tanner Y. Drug resistance mechanisms of FGFR-driven cancers. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2019. [cited 2021 Apr 18].
Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/56803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775329.
Council of Science Editors:
Tanner Y. Drug resistance mechanisms of FGFR-driven cancers. [Doctoral Dissertation]. Queen Mary, University of London; 2019. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/56803 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775329

Queen Mary, University of London
23.
Robbez-Masson, Luisa.
Investigating the functional significance of an FGFR2 intronic SNP in breast cancer.
Degree: PhD, 2013, Queen Mary, University of London
URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8539
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667133
► Single nucleotide polymorphisms present in the second intron of the fibroblast growth factor receptor 2 (FGFR2) gene have been linked with increased risk of breast…
(more)
▼ Single nucleotide polymorphisms present in the second intron of the fibroblast growth factor receptor 2 (FGFR2) gene have been linked with increased risk of breast cancer in several genome wide association studies. The potential effect of those SNPs appeared to be mediated through the differential binding of cis-regulatory elements, such as transcription factors, since all the SNPs in linkage disequilibrium were located in a regulatory DNA region. Preliminary studies have shown that a Runx2 binding site is functional only in the minor, disease associated allele of rs2981578, resulting in increased expression of FGFR2 in cancers from patients homozygous for that allele. Moreover, the increased risk conferred by the minor FGFR2 allele is associated most strongly in oestrogen receptor alpha positive (ERα) breast tumours, suggesting a potential interaction between ERα and FGFR signalling. Here, we have developed a human cell line model system to study the effect of those SNPs on cell behaviour. In an ERα positive breast cancer cell line, rs2981578 was edited using Zinc Finger Nucleases. Unexpectedly, the acquisition of the single risk allele in MCF7 cells failed to affect proliferation or cell cycle progression. Binding of Runx2 to the risk allele was not observed. However FOXA1 binding, an important ERα partner, appeared decreased at the rs2981578 locus in the risk allele cells. Additionally, differences in allele specific expression (ASE) of FGFR2 were not observed in a panel of 72 ERα positive breast cancer samples. Thus, the apparent increased risk of developing ERα positive breast cancer is not caused by rs2981578 alone. Rather, the observed increased risk of developing breast cancer might be the result of a coordinated effect of multiple SNPs forming a risk haplotype in the second intron of FGFR2.
Subjects/Keywords: 616.99; Medicine; Cancer; Breast cancer; Fibroblast growth factor receptor 2 (FGFR2)
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Robbez-Masson, L. (2013). Investigating the functional significance of an FGFR2 intronic SNP in breast cancer. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/8539 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667133
Chicago Manual of Style (16th Edition):
Robbez-Masson, Luisa. “Investigating the functional significance of an FGFR2 intronic SNP in breast cancer.” 2013. Doctoral Dissertation, Queen Mary, University of London. Accessed April 18, 2021.
http://qmro.qmul.ac.uk/xmlui/handle/123456789/8539 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667133.
MLA Handbook (7th Edition):
Robbez-Masson, Luisa. “Investigating the functional significance of an FGFR2 intronic SNP in breast cancer.” 2013. Web. 18 Apr 2021.
Vancouver:
Robbez-Masson L. Investigating the functional significance of an FGFR2 intronic SNP in breast cancer. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2013. [cited 2021 Apr 18].
Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8539 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667133.
Council of Science Editors:
Robbez-Masson L. Investigating the functional significance of an FGFR2 intronic SNP in breast cancer. [Doctoral Dissertation]. Queen Mary, University of London; 2013. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8539 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667133

IUPUI
24.
Bonfitto, Anna.
Testing bone cell models responsive to a soluble form of klotho.
Degree: 2016, IUPUI
URL: http://hdl.handle.net/1805/11872
► Indiana University-Purdue University Indianapolis (IUPUI)
Fibroblast growth factor-23 (FGF23) is a hormone produced in bone that acts upon the kidney to control blood phosphate and…
(more)
▼ Indiana University-Purdue University Indianapolis (IUPUI)
Fibroblast growth factor-23 (FGF23) is a hormone produced in bone that acts upon the kidney to control blood phosphate and 1,25-(OH)2 vitamin D concentrations. Chronic kidney disease-mineral bone disorder (CKD-MBD) is a major public health problem, affecting 1 in 8 individuals. These patients can have markedly elevated FGF23 at end stage disease which is associated with metabolic bone anomalies, left ventricular hypertrophy, as well as increased mortality (>6-fold). The FGF23 co-receptor αKlotho (αKL) is a membrane-bound protein (mKL) that forms heteromeric complexes with FGF receptors (FGFRs) to initiate intracellular signaling. It also circulates as a cleavage product of mKL (‘cleaved’, or cKL). Previously, a patient with increased plasma cKL from a balanced translocation between chromosomes 9 and 13 in the KLOTHO gene presented with metabolic bone disease and a complex endocrine profile, despite hypophosphatemia. The lack of a reliable cell model in which to study potential FGF23-cKL interactions is a major hurdle for the field of phosphate metabolism. The goal of the present studies was to test and characterize bone cell lines that may respond to FGF23 and/or cKL, permitting study of novel aspects of phosphate handling and control of FGF23 expression. It was confirmed that stable delivery of cKL via AAV2/8 to wild type (WT) and KL-KO mice resulted in highly elevated bone FGF23 mRNA. MC3T3 (mouse) and ROS (rat) osteoblastic cell lines were tested for p-ERK1/2 responses to control FGFs, as well as FGF23 and cKL, alone or in combination. Importantly, both cell lines demonstrated responsiveness to FGF23+cKL only, and not the individual factors. To test responsiveness at the cell level, EGR1 mRNA was tested as an index of FGFR activity and showed modest increases with the same treatments, supporting that other factors may be required for full transcriptional effects. The present studies show that MC3T3 have FGF-dependent signaling capabilities, and that the combination of FGF23+cKL is required for efficient MAPK signaling. These results demonstrated that cKL provision is permissive for efficient FGF23 signaling in bone, and revealed important implications for the regulation of FGF23 and cKL in Mendelian, and common, genetic disorders of phosphate handling and biomineralization.
Advisors/Committee Members: White, Kenneth E..
Subjects/Keywords: Fibroblast growth factor-23; Klotho; Phosphate metabolism; MC3T3
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bonfitto, A. (2016). Testing bone cell models responsive to a soluble form of klotho. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/11872
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Bonfitto, Anna. “Testing bone cell models responsive to a soluble form of klotho.” 2016. Thesis, IUPUI. Accessed April 18, 2021.
http://hdl.handle.net/1805/11872.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Bonfitto, Anna. “Testing bone cell models responsive to a soluble form of klotho.” 2016. Web. 18 Apr 2021.
Vancouver:
Bonfitto A. Testing bone cell models responsive to a soluble form of klotho. [Internet] [Thesis]. IUPUI; 2016. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/1805/11872.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Bonfitto A. Testing bone cell models responsive to a soluble form of klotho. [Thesis]. IUPUI; 2016. Available from: http://hdl.handle.net/1805/11872
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Manitoba
25.
Koleini, Navid.
The role of high molecular weight fibroblast growth factor-2 in cardiac response to injury.
Degree: Physiology and Pathophysiology, 2019, University of Manitoba
URL: http://hdl.handle.net/1993/34449
► Fibroblast growth factor-2 (FGF2) is a multifunctional protein expressed as 18 kDa, low molecular weight (Lo-FGF2), and >20 kDa, high molecular weight (Hi-FGF2) isoforms with…
(more)
▼ Fibroblast growth factor-2 (FGF2) is a multifunctional protein expressed as 18 kDa, low molecular weight (Lo-FGF2), and >20 kDa, high molecular weight (Hi-FGF2) isoforms with potentially distinct biological functions. In the current thesis we have investigated the general hypothesis that the FGF2 isoforms exert distinct long- term effects towards cardiac response to injurious stimuli.
Administration of recombinant Lo- or Hi-FGF2 were equally effective in attenuating acute Doxorubicin (Dox)-induced cardiomyocyte damage and cell death in vitro, through the activation of mTOR/Nrf2/Heme oxygenase-1 pathway. Additionally, it was documented that a non-mitogenic, non-angiogenic mutant form of Lo-FGF2, carrying a serine-to-alanine, S117A, substitution, retained the cardioprotective properties against Dox.
A genetic mouse model lacking endogenous Hi-FGF2 (but not Lo-FGF2) expression, FGF2(Lo) was found to be protected from Dox-induced decline in contractile function, at 10 days post-Dox injection, as assessed by echocardiography, in both male and female mice. Wild type mice showed the expected decline in cardiac function post-Dox. Neutralizing anti-Hi-FGF2 antibodies, furthermore, were able to attenuate Dox-induced damage in cardiomyocytes co-cultured with wild type fibroblasts. Thus, elimination of endogenous Hi-FGF2, or neutralization of secreted, paracrine Hi-FGF2, increases cardiomyocyte resistance to Dox exposure.
Using transverse aortic constriction (TAC) surgery to induced pressure overload it was found that genetic elimination of Hi-FGF2 prevented the decline in systolic function, the increases in cardiac stress markers, and increases in cardiomyocyte size, present in FGF2 (WT) mice at 4-8 weeks post-TAC. In contrast, diastolic dysfunction, fibrosis, and cardiac mass enlargement post-TAC were found to be independent of endogenous Hi-FGF2. Whole cardiac transcriptome analysis revealed increased expression of the cardioprotective heat shock 70 (HSP70) protein in the absence of endogenous Hi-FGF2. In addition, genes involved in modulation of the circadian rhythm, most prominently the nuclear receptor NR1D1, may also contribute to the protected phenotype of the FGF2(Lo) mice, as they were differentially regulated post-TAC depending on the presence or absence of endogenous Hi-FGF2.
Work presented here shows that endogenous Hi-FGF2 aggravates cardiac response to two major causes of heart failure, Dox-toxicity and pressure overload. Neutralization of paracrine Hi-FGF2 through an antibody-based approach is a possible therapeutic approach against these pathologies.
Advisors/Committee Members: Kardami, Elissavet (Physiology and Pathophysiology) (supervisor), Dixon, Ian (Physiology and Pathophysiology) Czubryt, Michael (Physiology and Pathophysiology) Kirshenbaum, Lorrie (Physiology and Pathophysiology) Wigle, Jeffery (Biochemistry and Medical Genetics) Oudit, Gavin (University of Alberta) (examiningcommittee).
Subjects/Keywords: Fibroblast Growth Factor 2; Doxorubicin cardiotoxicity; Pressure overload cardiac injury
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Koleini, N. (2019). The role of high molecular weight fibroblast growth factor-2 in cardiac response to injury. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/34449
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Koleini, Navid. “The role of high molecular weight fibroblast growth factor-2 in cardiac response to injury.” 2019. Thesis, University of Manitoba. Accessed April 18, 2021.
http://hdl.handle.net/1993/34449.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Koleini, Navid. “The role of high molecular weight fibroblast growth factor-2 in cardiac response to injury.” 2019. Web. 18 Apr 2021.
Vancouver:
Koleini N. The role of high molecular weight fibroblast growth factor-2 in cardiac response to injury. [Internet] [Thesis]. University of Manitoba; 2019. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/1993/34449.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Koleini N. The role of high molecular weight fibroblast growth factor-2 in cardiac response to injury. [Thesis]. University of Manitoba; 2019. Available from: http://hdl.handle.net/1993/34449
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Southern California
26.
Utley, Sarah.
The role of fibroblast growth factor signaling on postnatal
hepatic progenitor cell expansion.
Degree: PhD, Systems Biology and Disease, 2015, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/285763/rec/7223
► Fibroblast Growth Factor (FGF) signaling is an established regulator of endoderm specification to the hepatic fate. We have previously determined that Fibroblast Growth Factors (FGFs)…
(more)
▼ Fibroblast Growth Factor (FGF) signaling is an
established regulator of endoderm specification to the hepatic
fate. We have previously determined that
Fibroblast Growth Factors
(FGFs) promote the proliferation and survival of embryonic hepatic
progenitor cells (HPCs), termed hepatoblasts, and a transformed
murine HPC line via AKT-dependent β-catenin activation. Recent
studies have shown that postnatal expansion of A6-expressing HPCs
during 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) induced
liver injury is partly mediated by β-catenin activation and FGF
signaling. Herein, we examine the role of FGF signaling in early
postnatal HPCs and acute DDC-induced HPC expansion. Methods: The
effects of FGF10 on early postnatal HPCs was studied by inducible
transgenic pups over-expressing Fgf10 (P21 Fgf10 Induced) from
postnatal day 7 (P7) to P21. For postnatal liver injury, inducible
transgenic mice were fed 0.1% DDC chow for 14 days concurrent with
either over-activation of FGF signaling by Fgf10 over-expression or
inhibition of FGF signaling via dominant-negative expression of
soluble FGF Receptor (R)-2IIIb. Results: During early postnatal
development, a resident population of cells with a high nuclei-to
cytoplasmic ratio increases from postnatal day 0 (P0) through P7
before it disappears histologically. Over-expression of Fgf10 from
P7 to P21 retains and expands the periportal cell population which
normally declines after P7. Characterization of this cell
population revealed they express HPC markers CD49f, and CD133, but
lack expression of markers for mesenchymal cells, differentiated
hepatocytes and biliary epithelial cells. This heterogeneous cell
population expressed epithelial cell marker E-Cadherin, and a
subset of the cells was CD45 positive, indicating infiltration of
hematopoietic cells as well. During acute postnatal DDC injury, we
observed expansion of cells expressing FGFR1 and FGFR2 in the
periportal ductular reaction. Quantitative PCR analysis of the
non-hepatocyte cell fraction demonstrated significant up-regulation
of genes encoding FGFR2IIIb ligands: Fgf7, Fgf10, and Fgf22.
Over-expression of Fgf10 increased the number of cells co-positive
for HPC marker A6 and hepatocyte marker HEPATOCYTE NUCLEAR
FACTOR-4α (HNF4α) while reducing serum total bilirubin.
Dominant-negative FGFR pathway inhibition reduced the number of
periportal cells exhibiting AKT-dependent activation of β-catenin,
and changed the distribution of cells co-expressing A6 and HNF4α by
reducing dual positive cells near the central vein of the hepatic
lobule while increasing them near the portal vein. Co-treatment of
Fgf10 over-expressing DDC-treated mice with AKT inhibitor
Wortmannin similarly changed the distribution of A6/HNF4α
co-positive cells. Conclusion: FGF signaling regulates the
expansion of early postnatal hepatic progenitor cells and
DDC-induced A6-expressing hepatocytes partly through AKT-dependent
activation of β-catenin.
Advisors/Committee Members: Wang, Kasper (Committee Chair), Warburton, David (Committee Member), DeLeve, Laurie (Committee Member), Frey, Mark R. (Committee Member).
Subjects/Keywords: fibroblast growth factor; hepatic progenitor cells; beta-catenin
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Utley, S. (2015). The role of fibroblast growth factor signaling on postnatal
hepatic progenitor cell expansion. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/285763/rec/7223
Chicago Manual of Style (16th Edition):
Utley, Sarah. “The role of fibroblast growth factor signaling on postnatal
hepatic progenitor cell expansion.” 2015. Doctoral Dissertation, University of Southern California. Accessed April 18, 2021.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/285763/rec/7223.
MLA Handbook (7th Edition):
Utley, Sarah. “The role of fibroblast growth factor signaling on postnatal
hepatic progenitor cell expansion.” 2015. Web. 18 Apr 2021.
Vancouver:
Utley S. The role of fibroblast growth factor signaling on postnatal
hepatic progenitor cell expansion. [Internet] [Doctoral dissertation]. University of Southern California; 2015. [cited 2021 Apr 18].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/285763/rec/7223.
Council of Science Editors:
Utley S. The role of fibroblast growth factor signaling on postnatal
hepatic progenitor cell expansion. [Doctoral Dissertation]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/285763/rec/7223

University of Melbourne
27.
Tan, Sven Jean.
Phosphate handling in kidney disease: the role of klotho and fibroblast growth factor-23.
Degree: 2016, University of Melbourne
URL: http://hdl.handle.net/11343/123415
► Derangement in phosphate control has long been considered central to the pathophysiological processes leading to chronic kidney disease-mineral bone disorder (CKD-MBD). Discovery of two phosphate…
(more)
▼ Derangement in phosphate control has long been considered central to the pathophysiological processes leading to chronic kidney disease-mineral bone disorder (CKD-MBD). Discovery of two phosphate regulatory proteins, fibroblast growth factor-23 (FGF-23) and α-klotho, has broadened our understanding of mineral metabolism and phosphate handling. The clinical studies in this thesis examined the impact of CKD, unilateral donor nephrectomy and kidney transplantation respectively on circulating FGF-23 and soluble-klotho levels, while basic science studies were performed to determine in vivo expression of klotho in the human kidney as well as to elucidate klotho’s reno-protective properties in vitro.
Subjects/Keywords: klotho; fibroblast growth factor-23; phosphate; kidney disease
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Tan, S. J. (2016). Phosphate handling in kidney disease: the role of klotho and fibroblast growth factor-23. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/123415
Chicago Manual of Style (16th Edition):
Tan, Sven Jean. “Phosphate handling in kidney disease: the role of klotho and fibroblast growth factor-23.” 2016. Doctoral Dissertation, University of Melbourne. Accessed April 18, 2021.
http://hdl.handle.net/11343/123415.
MLA Handbook (7th Edition):
Tan, Sven Jean. “Phosphate handling in kidney disease: the role of klotho and fibroblast growth factor-23.” 2016. Web. 18 Apr 2021.
Vancouver:
Tan SJ. Phosphate handling in kidney disease: the role of klotho and fibroblast growth factor-23. [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/11343/123415.
Council of Science Editors:
Tan SJ. Phosphate handling in kidney disease: the role of klotho and fibroblast growth factor-23. [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/123415

University of Georgia
28.
Esposito, Tina.
Placentation in the bovine with specific emphasis on the role of the trophoblast cells and placental abnormalities associated with the nuclear transfer process.
Degree: 2014, University of Georgia
URL: http://hdl.handle.net/10724/20539
► Placental abnormalities are proving to be a formidable obstacle to overcome in the nuclear transfer process. In the bovine, it is the trophoblast cells which…
(more)
▼ Placental abnormalities are proving to be a formidable obstacle to overcome in the nuclear transfer process. In the bovine, it is the trophoblast cells which make the major contribution to the parenchyma cells of the placenta. Previous
studies have shown trophoblast cells to be feeder layer dependent, and, in the mouse, fibroblast growth factor-4 dependent, to remain undifferentiated and in a proliferating state. To date, t here have been no reports o f a bovine trophoblast cell line
that is not feeder layer dependent, nor are there any studies determining the effects of fibroblast growth factor-4 on bovine trophoblast. It would be useful to have a stable line of bovine trophoblast cells, for in vitro studies, to determine if these
cells are capable o f contributing the trophectoderm lineage in vitro, and eventually in vivo, t o aid in development of a normal, functioning placenta.
Subjects/Keywords: Placenta; Bovine; Trophoblast; Fibroblast growth factor-4; Nuclear transfer; Feeder layers
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Esposito, T. (2014). Placentation in the bovine with specific emphasis on the role of the trophoblast cells and placental abnormalities associated with the nuclear transfer process. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/20539
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Esposito, Tina. “Placentation in the bovine with specific emphasis on the role of the trophoblast cells and placental abnormalities associated with the nuclear transfer process.” 2014. Thesis, University of Georgia. Accessed April 18, 2021.
http://hdl.handle.net/10724/20539.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Esposito, Tina. “Placentation in the bovine with specific emphasis on the role of the trophoblast cells and placental abnormalities associated with the nuclear transfer process.” 2014. Web. 18 Apr 2021.
Vancouver:
Esposito T. Placentation in the bovine with specific emphasis on the role of the trophoblast cells and placental abnormalities associated with the nuclear transfer process. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/10724/20539.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Esposito T. Placentation in the bovine with specific emphasis on the role of the trophoblast cells and placental abnormalities associated with the nuclear transfer process. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/20539
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Tech
29.
Damico, Carmen Marie.
A Microfludic Assay Device for Study of Cell Migration on ECM-mimicking Suspended Nanofibers in Presence of Biochemical Cues.
Degree: MS, Mechanical Engineering, 2016, Virginia Tech
URL: http://hdl.handle.net/10919/82003
► Eukaryotic cell chemotaxis, or directed cell migration in response to a chemoeffector gradient, plays a central role in many important biological process such as wound…
(more)
▼ Eukaryotic cell chemotaxis, or directed cell migration in response to a chemoeffector gradient, plays a central role in many important biological process such as wound healing, cancer metastasis, and embryogenesis. In vivo, cells migrate on fibrous ECM, but chemotaxis studies are typically conducted on flat substrates which fail to recapitulate ECM or 3D gel environments with heterogeneous and poorly defined biophysical properties.
To address these challenges, this thesis focused on developing a microfluidic assay device which utilizes a reductionist approach to study single cell chemotaxis on aligned, suspended ECM-mimicking nanofibers. The device is comprised of a network of microfluidic mixing channels which produce a temporally invariant, linear chemical gradient over nanofiber scaffolds in an observation channel. The microfluidic device design was guided by a numerical model and validated with experimental testing. This device was used to study mouse embryonic
fibroblast NIH/3T3 response to platelet derived
growth factor (PDGF) on flat polystyrene and suspended, polystyrene nanofibers with small (15 μm), and large (25 μm) spacing. Cell aspect ratio is lowest for flat polystyrene (spread morphology) and highest for large-spaced fibers (spindle morphology). Cells migrating on fibers begin to show a chemotaxis response to a PDGF gradient 10 times shallower than that required for chemotaxis response on a flat substrate. Furthermore, cells with spindle morphology maintain a robust and strong response over a broad range of chemoattractant concentration. These cells also had a 45% increase in speed and 26% increase in persistence over cells on flat polystyrene. The findings of this thesis suggest that 2D substrates may not be sufficient for studying physiologically relevant chemotaxis.
Advisors/Committee Members: Behkam, Bahareh (committeechair), Nain, Amrinder (committee member), Paul, Mark R. (committee member).
Subjects/Keywords: mesenchymal chemotaxis; biophysical-biochemical cues; fibroblast; platelet-derived growth factor
Record Details
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Damico, C. M. (2016). A Microfludic Assay Device for Study of Cell Migration on ECM-mimicking Suspended Nanofibers in Presence of Biochemical Cues. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/82003
Chicago Manual of Style (16th Edition):
Damico, Carmen Marie. “A Microfludic Assay Device for Study of Cell Migration on ECM-mimicking Suspended Nanofibers in Presence of Biochemical Cues.” 2016. Masters Thesis, Virginia Tech. Accessed April 18, 2021.
http://hdl.handle.net/10919/82003.
MLA Handbook (7th Edition):
Damico, Carmen Marie. “A Microfludic Assay Device for Study of Cell Migration on ECM-mimicking Suspended Nanofibers in Presence of Biochemical Cues.” 2016. Web. 18 Apr 2021.
Vancouver:
Damico CM. A Microfludic Assay Device for Study of Cell Migration on ECM-mimicking Suspended Nanofibers in Presence of Biochemical Cues. [Internet] [Masters thesis]. Virginia Tech; 2016. [cited 2021 Apr 18].
Available from: http://hdl.handle.net/10919/82003.
Council of Science Editors:
Damico CM. A Microfludic Assay Device for Study of Cell Migration on ECM-mimicking Suspended Nanofibers in Presence of Biochemical Cues. [Masters Thesis]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/82003

Hong Kong University of Science and Technology
30.
Kwong, Wai Yeung.
Novel recombinant DNA approaches engineered for the production of commercially valuable proteins.
Degree: 2013, Hong Kong University of Science and Technology
URL: http://repository.ust.hk/ir/Record/1783.1-80935
;
https://doi.org/10.14711/thesis-b1254355
;
http://repository.ust.hk/ir/bitstream/1783.1-80935/1/th_redirect.html
► Extracellular production of recombinant proteins using bacterial systems may enable the proteins concerned to retain important properties including structural authenticity and functional activity. By employing…
(more)
▼ Extracellular production of recombinant proteins using bacterial systems may enable the proteins concerned to retain important properties including structural authenticity and functional activity. By employing a secretory approach together with the Bacillus subtilis veg-expression-system, an alluring yield of human basic fibroblast growth factor (hbFGF), which had never been expressed as an authentic protein in recombinant approach, was successfully achieved by me as protein secreted in the culture supernatant. However, despite the secretory nature of hbFGF, it has not been successfully expressed through excretion in Escherichia coli. With the development and application of a novel intein-mediated-cleavage-excretory system, I was able to demonstrate, for the first time, excretory production of both hbFGF and human epidermal growth factor (hEGF) in the same E. coli host. Both the growth factors, existing in their mature authentic structures, were detected in both the cell lysate and culture medium fractions. Furthermore, making use of the same intein-mediated-cleavage excretory system, high levels of endoglucanase A of Cellulomonas fimi and hEGF were co-produced in the E. coli host, supporting the conclusion that the system may serve as a versatile platform for use in the co-expression of proteins with widely different origins and properties. Despite the merits of extracellular expression, hyper-expression of the secretory proteins often results in severe cell death. A novel strategy consisted of the use of an intein-mediated-cleavage system and “delayed” secretion of the precursor protein, was developed. By fusing the DnaB mini-intein at the N-terminus of the OmpA signal peptide of an exoglucanase (Exg), the cell death and plasmid curing caused by secretory Exg was decreased, leading to a significant improvement in the yield of excreted Exg. The various novel expression strategies introduced in above and discussed in this dissertation may prove to be applicable for cost-effective production of a wide range of valuable proteins.
Subjects/Keywords: Bacillus subtilis
; Escherichia coli
; Secretion
; Fibroblast growth factors
; Epidermal growth factor
; Recombinant proteins
; Therapeutic use
Record Details
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kwong, W. Y. (2013). Novel recombinant DNA approaches engineered for the production of commercially valuable proteins. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-80935 ; https://doi.org/10.14711/thesis-b1254355 ; http://repository.ust.hk/ir/bitstream/1783.1-80935/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kwong, Wai Yeung. “Novel recombinant DNA approaches engineered for the production of commercially valuable proteins.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed April 18, 2021.
http://repository.ust.hk/ir/Record/1783.1-80935 ; https://doi.org/10.14711/thesis-b1254355 ; http://repository.ust.hk/ir/bitstream/1783.1-80935/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kwong, Wai Yeung. “Novel recombinant DNA approaches engineered for the production of commercially valuable proteins.” 2013. Web. 18 Apr 2021.
Vancouver:
Kwong WY. Novel recombinant DNA approaches engineered for the production of commercially valuable proteins. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Apr 18].
Available from: http://repository.ust.hk/ir/Record/1783.1-80935 ; https://doi.org/10.14711/thesis-b1254355 ; http://repository.ust.hk/ir/bitstream/1783.1-80935/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kwong WY. Novel recombinant DNA approaches engineered for the production of commercially valuable proteins. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-80935 ; https://doi.org/10.14711/thesis-b1254355 ; http://repository.ust.hk/ir/bitstream/1783.1-80935/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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