subject:(Transcription factors)

University of Utah

1. Close, Devin W. Structural and Biochemical Studies of the Transcription Elongation Factors Spt6 and Tex.

Degree: PhD, Biochemistry;, 2010, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/719/rec/1086

► Proper gene expression relies on the precise coordination of cellular processes that influence packaging, transcription, and processing of the genetic material. Linkage and regulation of… (more)

▼ Proper gene expression relies on the precise coordination of cellular processes that influence packaging, transcription, and processing of the genetic material. Linkage and regulation of these processes is organized by factors that remodel and modify nucleosomes, regulate transcription, and influence RNA processing and export. One of these factors, Spt6, is a large (~168kDa), essential, highly conserved, and functionally diverse eukaryotic protein. Best known as a histone chaperone capable of altering the structure of nucleosomes, Spt6 has also been shown to function as a transcription elongation factor as well as a critical component for proper RNA processing. Although a broader role for Spt6 is reasonably well-understood, very little is known about the functional and mechanistic details of this multifaceted protein. Beyond studying Spt6 directly, insight into Spt6 function may come from complimentary studies on the bacterial protein Tex. Tex is a transcription elongation factor predicted to be a structurally similar to Spt6. The function of Tex is not well-understood, but may be functioning in a homologous manner to Spt6 in two vastly different transcriptional environments. In order to gain insight into the mechanism of Spt6 and Tex, the work presented in this thesis has focused on structural and biochemical studies of Spt6 from Saccharomyces cerevisiae and the related Tex protein from Pseudomonas aeruginosa. To this end, several Spt6 crystal structures have been determined resulting in a nearly complete composite model for Spt6. Along with a series of domains predicted to mediate protein and nucleic acid interactions, the structure reveals a novel tandem SH2 domain consisting of the only two SH2 folds known in yeast. Biochemical analysis of Spt6 demonstrates its capacity to interact with an array of functionally relevant protein and nucleic acid substrates which provide clues into mechanisms underlying the various functions of Spt6. Parallel studies on Tex demonstrate a strikingly similar structure and domain architecture to that of the Spt6 core. Structural and biochemical work described in this thesis lays the foundation for further in vitro and in vivo studies aimed at a better understanding of how Spt6 and Tex regulate gene expression. The highly similar core structure shared between Spt6 and Tex may ultimately prove to be a protein scaffold for regulating transcription in both eukaryotic and prokaryotic organisms.

Subjects/Keywords: Transcription Factors

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APA (6^th Edition):

Close, D. W. (2010). Structural and Biochemical Studies of the Transcription Elongation Factors Spt6 and Tex. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/719/rec/1086

Chicago Manual of Style (16^th Edition):

Close, Devin W. “Structural and Biochemical Studies of the Transcription Elongation Factors Spt6 and Tex.” 2010. Doctoral Dissertation, University of Utah. Accessed July 21, 2019. http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/719/rec/1086.

MLA Handbook (7^th Edition):

Close, Devin W. “Structural and Biochemical Studies of the Transcription Elongation Factors Spt6 and Tex.” 2010. Web. 21 Jul 2019.

Vancouver:

Close DW. Structural and Biochemical Studies of the Transcription Elongation Factors Spt6 and Tex. [Internet] [Doctoral dissertation]. University of Utah; 2010. [cited 2019 Jul 21]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/719/rec/1086.

Council of Science Editors:

Close DW. Structural and Biochemical Studies of the Transcription Elongation Factors Spt6 and Tex. [Doctoral Dissertation]. University of Utah; 2010. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd2/id/719/rec/1086

Oregon State University

2. Bhattacharya, Shreya. Transcription factor CTIP2 regulates hair follicle development, hair cycling and wound healing.

Degree: PhD, Molecular and Cellular , 2014, Oregon State University

URL: http://hdl.handle.net/1957/50364

► The integumentary system is the largest organ system of the body that comprises of skin and its appendages such as hair follicles, sebaceous and sweat… (more)

▼ The integumentary system is the largest organ system of the body that comprises of skin and its appendages such as hair follicles, sebaceous and sweat glands. Skin is divided into three distinct structural layers: the epidermis, dermis and hypodermis. The epidermis originates from the ectoderm and is composed of four layers specified as basal, spinous, granular and corneal layer. The function of epidermis is to protect against all sources of environmental insults, prevent water loss and undergo re-epithelialization after wounding. For its normal functioning, the epidermis continually replenishes itself through a process of continuous proliferation and terminal differentiation of keratinocytes from the basal layer. The hair follicle is a complex appendage of skin, which give rise to the keratinized hair shaft. Hair follicle is formed during embryonic development and it goes through cycles of growth (anagen), regression (catagen) and quiescence (telogen). The bulge region of the hair follicle in the outer root sheath area contains slow-cycling stem cells which are responsible for normal hair cycling as well as cutaneous wound repair after injury. CTIP2 (COUP-TF interacting protein 2) is a C2H2 zinc finger transcription factor that is expressed in various organs and tissues. It has been shown to play an important role in the development of thymocyte, tooth and corticospinal motor neuron. Expression of CTIP2 is observed in the developing murine epidermis and dermis during skin organogenesis and predominantly in epidermal keratinocytes in adult mice skin. It is also expressed in the embryonic and mature adult hair follicles, especially in bulge region. CTIP2 regulates epidermal proliferation and terminal differentiation during embryogenesis and adulthood. Here we show that CTIP2 controls hair follicle development, hair cycling and cutaneous wound healing. To study the role of CTIP2 in hair morphogenesis and hair cycling, we have utilized two different genetically modified mouse strains. First, we studied the effect of CTIP2 during hair follicle formation using Ctip2-null mice containing a germline deletion of Ctip2. Ctip2-null mice exhibited reduced hair follicle density and downregulation of EGFR and NOTCH1 expression. To analyze the consequence of loss-of–funtion of CTIP2 on postnatal hair cycling, we selectively ablated Ctip2 in the epidermis and hair follicles using the Cre-LoxP strategy to generate Ctip2[superscript ep-/-] mice. Ctip2[superscript ep-/-] mice showed a defect in postnatal hair cycling marked by early exit from telogen and premature entry into anagen. The premature induction of anagen is a result of stem cell activation, increase in cell proliferation and decrease in apoptosis-driven cell death in the hair follicles. This early activation of follicular stem cells eventually leads to their depletion and therefore ultimate loss of hair follicles and hair coat. Reduced expression of LHX2 and NFATC1, which are two important regulators of hair cycling, was observed in the bulge area of Ctip2[superscript… Advisors/Committee Members: Indra, Arup K. (advisor), Leid, Mark (committee member).

Subjects/Keywords: Transcription factors

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APA (6^th Edition):

Bhattacharya, S. (2014). Transcription factor CTIP2 regulates hair follicle development, hair cycling and wound healing. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/50364

Chicago Manual of Style (16^th Edition):

Bhattacharya, Shreya. “Transcription factor CTIP2 regulates hair follicle development, hair cycling and wound healing.” 2014. Doctoral Dissertation, Oregon State University. Accessed July 21, 2019. http://hdl.handle.net/1957/50364.

MLA Handbook (7^th Edition):

Bhattacharya, Shreya. “Transcription factor CTIP2 regulates hair follicle development, hair cycling and wound healing.” 2014. Web. 21 Jul 2019.

Vancouver:

Bhattacharya S. Transcription factor CTIP2 regulates hair follicle development, hair cycling and wound healing. [Internet] [Doctoral dissertation]. Oregon State University; 2014. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1957/50364.

Council of Science Editors:

Bhattacharya S. Transcription factor CTIP2 regulates hair follicle development, hair cycling and wound healing. [Doctoral Dissertation]. Oregon State University; 2014. Available from: http://hdl.handle.net/1957/50364

Oregon State University

3. Kyrylkova, Kateryna. The role of the transcriptional regulatory protein BCL11B in dental and craniofacial development.

Degree: PhD, Pharmacy, 2014, Oregon State University

URL: http://hdl.handle.net/1957/45238

► BCL11B is a transcriptional regulatory protein that plays essential roles during mouse embryonic development. BCL11B is expressed and functions in the immune and nervous systems… (more)

▼ BCL11B is a transcriptional regulatory protein that plays essential roles during mouse embryonic development. BCL11B is expressed and functions in the immune and nervous systems as well as within ectodermal organs. Multiple studies have characterized the roles of BCL11B in T cells, brain, and skin. However, very little is known about the mechanistic role of BCL11B during tooth development, and data are not available on the function of BCL11B in the craniofacial skeleton. BCL11B is expressed widely within the oral cavity during development, and mice lacking BCL11B exhibit a spectrum of tooth developmental defects. The most striking feature of the Bcl11b[superscript -/-] dental phenotype is a defect in development of enamel-secreting cells, known as ameloblasts, in the mouse incisor. Ameloblasts are localized exclusively on the labial aspect of the mouse incisor in wild-type mice. In contrast, Bcl11b[superscript -/-] mice exhibit defective ameloblasts on the labial and develop ectopic, ameloblast-like cells on the lingual aspect of the tooth. BCL11B regulates asymmetric ameloblast formation by regulating the development of epithelial stem cell niches in the posterior part of the incisor. Specifically, BCL11B induces proliferation and differentiation of epithelial stem cells into ameloblasts in the labial cervical loop, whereas BCL11B suppresses these processes within the lingual epithelium. Such bidirectional actions of BCL11B are mediated by spatio-specific regulation of a large gene network comprised of genes that encode members of fibroblast growth factor (FGF) and transforming growth factor β (TGFβ) superfamilies, Sprouty proteins, and sonic hedgehog (SHH). In addition, my data integrate BCL11B into FGF and SHH signaling pathways revealing the molecular mechanisms that suppress development of ectopic ameloblast-like cells in the lingual epithelium. In the second half of this dissertation, I show that BCL11B is expressed in the osteogenic mesenchyme of developing craniofacial skeleton, and loss of BCL11B in these tissues has striking effects on craniofacial development. Bcl11b[superscript -/-] mice exhibit accelerated mineralization of the skull during embryonic development and synostosis of facial and coronal sutures. My results demonstrate that BCL11B normally functions to suppress proliferation and premature differentiation of osteoblasts in the craniofacial complex. I suggest that the principal mechanistic basis of these actions of BCL11B is the repression of Fgfr2c expression within the osteogenic mesenchyme. Taken together, my data demonstrate that BCL11B plays an important role in proliferation and differentiation of ameloblast and osteoblast lineages. In addition, my work implicates BCL11B in regulation of FGF and TGFβ signaling pathways. Therefore, these studies contribute to a better understanding of the molecular and cellular functions of BCL11B in vivo. Advisors/Committee Members: Leid, Mark (advisor), Kioussi, Chrissa (committee member).

Subjects/Keywords: Transcription factor; Transcription factors

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kyrylkova, K. (2014). The role of the transcriptional regulatory protein BCL11B in dental and craniofacial development. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/45238

Chicago Manual of Style (16^th Edition):

Kyrylkova, Kateryna. “The role of the transcriptional regulatory protein BCL11B in dental and craniofacial development.” 2014. Doctoral Dissertation, Oregon State University. Accessed July 21, 2019. http://hdl.handle.net/1957/45238.

MLA Handbook (7^th Edition):

Kyrylkova, Kateryna. “The role of the transcriptional regulatory protein BCL11B in dental and craniofacial development.” 2014. Web. 21 Jul 2019.

Vancouver:

Kyrylkova K. The role of the transcriptional regulatory protein BCL11B in dental and craniofacial development. [Internet] [Doctoral dissertation]. Oregon State University; 2014. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1957/45238.

Council of Science Editors:

Kyrylkova K. The role of the transcriptional regulatory protein BCL11B in dental and craniofacial development. [Doctoral Dissertation]. Oregon State University; 2014. Available from: http://hdl.handle.net/1957/45238

University of Hong Kong

4. 成云; Cheng, Yun. β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H.

Degree: PhD, 2016, University of Hong Kong

URL: Cheng, Y. [成云]. (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5816255. ; http://dx.doi.org/10.5353/th_b5816255 ; http://hdl.handle.net/10722/237862

► CREB-H is an endoplasmic reticulum-tethered bZIP transcription factor, which critically regulates lipid homeostasis and gluconeogenesis in the liver. CREB-H is proteolytically activated by regulated intramembrane… (more)

▼ CREB-H is an endoplasmic reticulum-tethered bZIP transcription factor, which critically regulates lipid homeostasis and gluconeogenesis in the liver. CREB-H is proteolytically activated by regulated intramembrane proteolysis to generate a C-terminally truncated form known as CREB-H-ΔTC, which translocates to the nucleus to activate the expression of target genes. We have previously characterized the roles and regulation of CREB-H in hepatic physiology and pathology. As the physiologically active form of CREB-H, CREB-H-ΔTC is a fast turnover protein. However, the mechanism governing CREB-H-ΔTC destruction was not well understood. In this study, I report on β-TrCP-dependent ubiquitination and proteasomal degradation of CREB-H-ΔTC. β-TrCP is the substrate recognition subunit of the E3 ubiquitin ligase SCF^(β-TrCP), which catalyzes the ubiquitination of various transcription factors and cell cycle regulatory proteins. By modulating the steady-state level and activity of these key factors, β-TrCP plays an important role in cell cycle control, oncogenesis and metabolic regulation. In my study, I first verified that the degradation of CREB-H-ΔTC was mediated by lysine 48-linked polyubiquitination. This degradation was effectively inhibited by a proteasome inhibitor. In search of the E3 ubiquitin ligase catalyzing CREB-H-ΔTC ubiquitination, bioinformatic analysis was carried out and β-TrCP was singled out as a potential E3. In light of the importance of β-TrCP in CREB-H-ΔTC degradation, experimental validation was performed. CREB-H-ΔTC physically interacted with β-TrCP. Forced expression of β-TrCP increased the polyubiquitination and decreased the stability of CREB-H-ΔTC, whereas knockdown of β-TrCP had the opposite effect. These results indicated that CREB-H-ΔTC undergoes β-TrCP-dependent lysine 48-linked polyubiquitination and degradation. I went on to characterize the molecular details of β-TrCP-mediated ubiquitination and degradation of CREB-H-ΔTC. An evolutionarily conserved sequence, SDSGIS, which functions as the β-TrCP-binding motif, was identified in CREB-H. CREB-H-ΔTC lacking this motif was stabilized and resistant to β-TrCP-induced polyubiquitination. This motif was a phosphodegron and phosphorylation at its serine residues was required for β-TrCP recognition. Furthermore, two additional phosphorylation sites close to the phosphodegron were identified. Interestingly, mutational analysis suggested that dephosphorylation of the two sites increased the transcriptional activity of CREB-H-ΔTC. Based on these results, I propose a new model for the regulation of CREB-H-ΔTC ubiquitination and degradation through both inhibitory and activating phosphorylation. Taken together, my work not only provided experimental evidence for β-TrCP-mediated ubiquitination and degradation of the active form of CREB-H transcription factor, but also revealed a new intracellular signaling pathway by which its ubiquitination and degradation are regulated. My findings have implications in the development of new agents that either…

Subjects/Keywords: Transcription factors; Ubiquitin

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APA (6^th Edition):

成云; Cheng, Y. (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. (Doctoral Dissertation). University of Hong Kong. Retrieved from Cheng, Y. [成云]. (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5816255. ; http://dx.doi.org/10.5353/th_b5816255 ; http://hdl.handle.net/10722/237862

Chicago Manual of Style (16^th Edition):

成云; Cheng, Yun. “β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H.” 2016. Doctoral Dissertation, University of Hong Kong. Accessed July 21, 2019. Cheng, Y. [成云]. (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5816255. ; http://dx.doi.org/10.5353/th_b5816255 ; http://hdl.handle.net/10722/237862.

MLA Handbook (7^th Edition):

成云; Cheng, Yun. “β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H.” 2016. Web. 21 Jul 2019.

Vancouver:

成云; Cheng Y. β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. [Internet] [Doctoral dissertation]. University of Hong Kong; 2016. [cited 2019 Jul 21]. Available from: Cheng, Y. [成云]. (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5816255. ; http://dx.doi.org/10.5353/th_b5816255 ; http://hdl.handle.net/10722/237862.

Council of Science Editors:

成云; Cheng Y. β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. [Doctoral Dissertation]. University of Hong Kong; 2016. Available from: Cheng, Y. [成云]. (2016). β-TrCP-mediated ubiquitination and degradation of liver-enriched transcription factor CREB-H. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5816255. ; http://dx.doi.org/10.5353/th_b5816255 ; http://hdl.handle.net/10722/237862

Oregon State University

5. Smith, Eric Jonathan. Age-related loss of Nrf2, a novel mechanism for the potential attenuation of xenobiotic detoxification capacity.

Degree: PhD, Biochemistry and Biophysics, 2014, Oregon State University

URL: http://hdl.handle.net/1957/50007

► Nuclear Factor, Erythroid Derived 2, Like 2 (NFE2L2 or Nrf2) is the primary transcription factor in cellular defense against oxidative and xenobiotic stresses in higher… (more)

▼ Nuclear Factor, Erythroid Derived 2, Like 2 (NFE2L2 or Nrf2) is the primary transcription factor in cellular defense against oxidative and xenobiotic stresses in higher eukaryotes. This basic leucine zipper transcription factor regulates over 200 antioxidant, detoxification, and lipid metabolizing genes by binding to the Antioxidant Response Element (ARE; a cis-acting element) as a transcription enhancer. Our group, and others, have identified that the nuclear steady state levels of this highly inducible transcription factor declines with age which coincides with decreased expression of many ARE regulated genes. To elucidate the mechanism(s) involved in lowered Nrf2 levels we used hepatocytes isolated from young and old rats as a relevant cellular model that maintains the aging phenotype with respect to Nrf2 levels. Our results show that steady state Nrf2 levels decline by ~40% with age (N=4, p<0.05), which led us to investigate the multifaceted regulation of Nrf2 homeostasis. Specifically, analysis of Nrf2 mRNA levels, and the rate of Nrf2 protein turnover and translation were investigated. Surprisingly, Keap1-mediated degradation of Nrf2, its primary negative regulator, did not account for the age-related Nrf2 decline, nor did mRNA levels change with age. Rather, Nrf2 protein synthesis declines 5.3-fold with age (N=3, p<0.05). Furthermore, we identify that rno-miR-146a, a key inflammation regulating miRNA, both inhibits Nrf2 translation and increases significantly with age. Taken together, our data suggest that the age-related loss of Nrf2 stems from the loss of its translation and may be mediated through miR regulation. Our lab previously demonstrated in rats, that the age-related loss of Nrf2 consequentially attenuates synthesis and steady state levels of liver glutathione (GSH) synthesis and manifests as a diminished level of GSH. This antioxidant is the most abundant non-protein thiol in most cells and is pivotal for the detoxification of many xenobiotics. The rate-limiting enzyme in GSH synthesis, γ-glutamyl-cysteine ligase (Gcl), is composed of a catalytic (Gclc), and a modulatory (Gclm) subunit. In mice and humans, it is established that Nrf2, through the ARE, regulates Gclc expression. However, this had not been established in rats. From a bioinformatics analysis of the 5’ upstream sequence of the rat Gclc gene, we identified 3 putative AREs (ARE1, ARE3, and ARE4), and one cis-element containing the core but not the flanking nucleotides of the ARE (ARE2). Luciferase reporter plasmids containing each individual ARE were transfected into H4IIE rat hepatoma cells to test for ARE activity. Only one, designated “ARE4”, produced appreciable luciferase activity and was dependent on Nrf2 expression, suggesting that this ARE is a “true” enhancer element. Chromatin immunoprecipitation (ChIP) and qPCR identified that Nrf2 binds ARE4 but not ARE1-3. Further ChIP analysis identified that known partner transcription factors of Nrf2 (small maf, c-Jun and c-Fos) were also bound to ARE4. Taken together, our data… Advisors/Committee Members: Hagen, Tory M. (advisor), Ho, Emily (committee member).

Subjects/Keywords: Nrf2; Transcription factors

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APA (6^th Edition):

Smith, E. J. (2014). Age-related loss of Nrf2, a novel mechanism for the potential attenuation of xenobiotic detoxification capacity. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/50007

Chicago Manual of Style (16^th Edition):

Smith, Eric Jonathan. “Age-related loss of Nrf2, a novel mechanism for the potential attenuation of xenobiotic detoxification capacity.” 2014. Doctoral Dissertation, Oregon State University. Accessed July 21, 2019. http://hdl.handle.net/1957/50007.

MLA Handbook (7^th Edition):

Smith, Eric Jonathan. “Age-related loss of Nrf2, a novel mechanism for the potential attenuation of xenobiotic detoxification capacity.” 2014. Web. 21 Jul 2019.

Vancouver:

Smith EJ. Age-related loss of Nrf2, a novel mechanism for the potential attenuation of xenobiotic detoxification capacity. [Internet] [Doctoral dissertation]. Oregon State University; 2014. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1957/50007.

Council of Science Editors:

Smith EJ. Age-related loss of Nrf2, a novel mechanism for the potential attenuation of xenobiotic detoxification capacity. [Doctoral Dissertation]. Oregon State University; 2014. Available from: http://hdl.handle.net/1957/50007

University of Ottawa

6. Hryniuk, Alexa Kathryn. The Role of Cdx Transcription Factors in the Adult Intestine .

Degree: 2015, University of Ottawa

URL: http://hdl.handle.net/10393/32332

► The homeodomain transcription factor family of Cdx genes, Cdx1, Cdx2 and Cdx4, are known to play essential roles in many developmental processes including neural tube… (more)

Subjects/Keywords: Transcription factors; Intestine

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APA (6^th Edition):

Hryniuk, A. K. (2015). The Role of Cdx Transcription Factors in the Adult Intestine . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/32332

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hryniuk, Alexa Kathryn. “The Role of Cdx Transcription Factors in the Adult Intestine .” 2015. Thesis, University of Ottawa. Accessed July 21, 2019. http://hdl.handle.net/10393/32332.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hryniuk, Alexa Kathryn. “The Role of Cdx Transcription Factors in the Adult Intestine .” 2015. Web. 21 Jul 2019.

Vancouver:

Hryniuk AK. The Role of Cdx Transcription Factors in the Adult Intestine . [Internet] [Thesis]. University of Ottawa; 2015. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/10393/32332.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hryniuk AK. The Role of Cdx Transcription Factors in the Adult Intestine . [Thesis]. University of Ottawa; 2015. Available from: http://hdl.handle.net/10393/32332

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Portland State University

7. Eustis, Robyn Lynn. The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation.

Degree: MS(M.S.) in Biology, Biology, 2015, Portland State University

URL: https://pdxscholar.library.pdx.edu/open_access_etds/2522

► All sequenced archaeal genomes encode a general transcription factor, TFE, which is highly conserved and homologous to the alpha subunit of the eukaryotic transcription… (more)

Subjects/Keywords: Archaebacteria; Transcription factors; Genetic transcription; Biology

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APA (6^th Edition):

Eustis, R. L. (2015). The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation. (Masters Thesis). Portland State University. Retrieved from https://pdxscholar.library.pdx.edu/open_access_etds/2522

Chicago Manual of Style (16^th Edition):

Eustis, Robyn Lynn. “The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation.” 2015. Masters Thesis, Portland State University. Accessed July 21, 2019. https://pdxscholar.library.pdx.edu/open_access_etds/2522.

MLA Handbook (7^th Edition):

Eustis, Robyn Lynn. “The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation.” 2015. Web. 21 Jul 2019.

Vancouver:

Eustis RL. The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation. [Internet] [Masters thesis]. Portland State University; 2015. [cited 2019 Jul 21]. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/2522.

Council of Science Editors:

Eustis RL. The Role of Pyrococcus furiosus Transcription Factor E in Transcription Iniitiation. [Masters Thesis]. Portland State University; 2015. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/2522

Portland State University

8. Micorescu, Michael. The Function of an Alternate TFB from Pyrococus furiosus and the Orientation of the TFB B-reader within Archaeal Transcription Initiation Complexes.

Degree: PhD, Biology, 2010, Portland State University

URL: http://pdxscholar.library.pdx.edu/open_access_etds/278

► The genome of the hyperthermophile archaeon Pyrococcus furiosus encodes two transcription factor B (TFB) paralogs, one of which (TFB1) was previously characterized in transcription… (more)

▼ The genome of the hyperthermophile archaeon Pyrococcus furiosus encodes two transcription factor B (TFB) paralogs, one of which (TFB1) was previously characterized in transcription initiation. The second TFB (TFB2) is unusual in that it lacks recognizable homology to the archaeal TFB/eukaryotic TFIIB B-reader (also called the B-finger) motif. TFB2 functions, though poorly, in promoter-dependent transcription initiation. Domain swaps between TFB1 and TFB2 showed that the low activity of TFB2 is determined mainly by its N terminus. The low activity of TFB2 in promoter opening and transcription can be partially relieved by transcription factor E (TFE). The results indicate that the TFB N-terminal region, containing conserved Zn ribbon and B-finger motifs, is important in promoter opening and that TFE can compensate for defects in the N terminus through enhancement of promoter opening. Archaeal RNA polymerase requires two transcription factors for initiation: TBP, which binds to TATA boxes, and TFB, which binds TBP and DNA, recruits RNAP and helps initiate transcription. Archaeal TFBs usually contain a conserved B-reader sequence homologous to the eukaryotic B-reader motif in their N-terminal domains. This region is involved in the assembly of the transcription complex, promoter melting and in transcription start site determination but its position and orientation relative to promoter DNA during initiation is not clear. In this study the positioning of the TFB B-reader relative to DNA was determined by cross-linking using TFB variants substituted with photoactivatable unnatural amino acids. The results demonstrate that the B-reader is in close proximity to the transcription start site on the template but not the non-template strand in transcription initiation complexes. Furthermore, the position of the B-reader varies between closed and open promoter complexes, and between open promoter and early initiation complexes. Thus the archaeal B-reader sequence is poised to interact with promoter DNA in a dynamic fashion, and is likely playing a role in positioning the template-strand in an open pre-initiation complex. Advisors/Committee Members: Michael S. Bartlett.

Subjects/Keywords: RNA polymerases; Genetic transcription; Transcription factors

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APA (6^th Edition):

Micorescu, M. (2010). The Function of an Alternate TFB from Pyrococus furiosus and the Orientation of the TFB B-reader within Archaeal Transcription Initiation Complexes. (Doctoral Dissertation). Portland State University. Retrieved from http://pdxscholar.library.pdx.edu/open_access_etds/278

Chicago Manual of Style (16^th Edition):

Micorescu, Michael. “The Function of an Alternate TFB from Pyrococus furiosus and the Orientation of the TFB B-reader within Archaeal Transcription Initiation Complexes.” 2010. Doctoral Dissertation, Portland State University. Accessed July 21, 2019. http://pdxscholar.library.pdx.edu/open_access_etds/278.

MLA Handbook (7^th Edition):

Micorescu, Michael. “The Function of an Alternate TFB from Pyrococus furiosus and the Orientation of the TFB B-reader within Archaeal Transcription Initiation Complexes.” 2010. Web. 21 Jul 2019.

Vancouver:

Micorescu M. The Function of an Alternate TFB from Pyrococus furiosus and the Orientation of the TFB B-reader within Archaeal Transcription Initiation Complexes. [Internet] [Doctoral dissertation]. Portland State University; 2010. [cited 2019 Jul 21]. Available from: http://pdxscholar.library.pdx.edu/open_access_etds/278.

Council of Science Editors:

Micorescu M. The Function of an Alternate TFB from Pyrococus furiosus and the Orientation of the TFB B-reader within Archaeal Transcription Initiation Complexes. [Doctoral Dissertation]. Portland State University; 2010. Available from: http://pdxscholar.library.pdx.edu/open_access_etds/278

University of Hong Kong

9. Yuan, Yuan. Transcriptional regulation of mouse secretin receptor in hypothalamic cells.

Degree: PhD, 2011, University of Hong Kong

URL: Yuan, Y. [袁媛]. (2011). Transcriptional regulation of mouse secretin receptor in hypothalamic cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775293 ; http://dx.doi.org/10.5353/th_b4775293 ; http://hdl.handle.net/10722/174473

►

As a neuropeptide, both secretin and secretin receptor are expressed in the central nervous system (CNS). It has been revealed that the activities of… (more)

Subjects/Keywords: Genetic transcription - Regulation.; Secretin - Receptors.; Transcription factors.

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APA (6^th Edition):

Yuan, Y. (2011). Transcriptional regulation of mouse secretin receptor in hypothalamic cells. (Doctoral Dissertation). University of Hong Kong. Retrieved from Yuan, Y. [袁媛]. (2011). Transcriptional regulation of mouse secretin receptor in hypothalamic cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775293 ; http://dx.doi.org/10.5353/th_b4775293 ; http://hdl.handle.net/10722/174473

Chicago Manual of Style (16^th Edition):

Yuan, Yuan. “Transcriptional regulation of mouse secretin receptor in hypothalamic cells.” 2011. Doctoral Dissertation, University of Hong Kong. Accessed July 21, 2019. Yuan, Y. [袁媛]. (2011). Transcriptional regulation of mouse secretin receptor in hypothalamic cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775293 ; http://dx.doi.org/10.5353/th_b4775293 ; http://hdl.handle.net/10722/174473.

MLA Handbook (7^th Edition):

Yuan, Yuan. “Transcriptional regulation of mouse secretin receptor in hypothalamic cells.” 2011. Web. 21 Jul 2019.

Vancouver:

Yuan Y. Transcriptional regulation of mouse secretin receptor in hypothalamic cells. [Internet] [Doctoral dissertation]. University of Hong Kong; 2011. [cited 2019 Jul 21]. Available from: Yuan, Y. [袁媛]. (2011). Transcriptional regulation of mouse secretin receptor in hypothalamic cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775293 ; http://dx.doi.org/10.5353/th_b4775293 ; http://hdl.handle.net/10722/174473.

Council of Science Editors:

Yuan Y. Transcriptional regulation of mouse secretin receptor in hypothalamic cells. [Doctoral Dissertation]. University of Hong Kong; 2011. Available from: Yuan, Y. [袁媛]. (2011). Transcriptional regulation of mouse secretin receptor in hypothalamic cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775293 ; http://dx.doi.org/10.5353/th_b4775293 ; http://hdl.handle.net/10722/174473

University of Hong Kong

10. Wang, Shimeng. Characterization of a universal stress protein UspA1171 of Burkholderia caribensis MBA4.

Degree: M. Phil., 2016, University of Hong Kong

URL: http://hdl.handle.net/10722/249195

► Burkholderia caribensis MBA4 is able to utilize haloacetic acids as growth substrates. A key enzyme, dehalogenase Deh4a, that enables bioremediation of halogenated organic compounds, was… (more)

▼ Burkholderia caribensis MBA4 is able to utilize haloacetic acids as growth substrates. A key enzyme, dehalogenase Deh4a, that enables bioremediation of halogenated organic compounds, was isolated from MBA4. A haloacid operon, which consists the structural genes for Deh4a and a transporter, Deh4p, was identified and characterized. So far, the transcription of this operon was found to regulate negatively. However, the mechanism has not been fully understood. Recently, a protein designated as TetR6620, encoded by gene K788_006620, has been found to bind to DNA fragment containing 100-bp of upstream non-coding region of the haloacid operon. Previous study showed that cell extracts prepared from glycolate-grown MBA4 produced two retardation complexes, A & B. When gene K788_006620 was disrupted in a mutant, Ins6620, the formation of the retardation complex A was abolished. Moreover, when purified recombinant TetR6620 with an N-terminal histidine-tag was used in similar bandshift assay, at least two retardation complexes were detected. The mobilities of these complexes are different from that of complexes A & B identified previously. When recombinant TetR6620 was supplemented to cell extracts of glycolate-grown Ins6620, the formation of complex A was restored. These suggest that while TetR6620 is able to bind to the upstream non-coding region of the haloacid operon, it probably interacted with another protein to perform its binding activity. By means of pull-down experiment, a universal stress protein UspA1171, encode by gene K788_001171, was envisaged to interact with TetR6620. In this study, the role of UspA1171 was characterized. A K788_001171 disruptant was constructed. Plasmid pKNOCK-Cm was used as a backbone and a derivative containing part of K788_001171 was used to disrupt gene K788_001171 in MBA4. If UspA1171 is a repressor for the haloacid operon, then a disruptant will have a relieved expression of Deh4a in glycolate-grown cells. Quantitative RT-PCR will be used to determine the expression levels of deh4a. The results showed that the slow migrating retardation complex A, identified in wildtype MBA4, was not found in glycolate-grown Ins6620. The gene K788_001171 has been amplified from the genome of MBA4 and cloned into an E. coli expression vector pET-14b. The plasmid was constructed and used to express UspA1171 in E. coli BL21(DE3). The recombinant histidine-tagged UspA1171 was over-expressed, purified and used in immobilized-metal affinity chromatography (IMAC) to pull down proteins that might interact with it. In addition, UspA1171 was used in BS3 crosslinking experiments with TetR6620. Western blot analysis was used to verify their interaction. The IMAC results showed that a 24 kDa protein was successfully pulled down from glycolate-grown Ins1171 by UspA1171 conjugated Ni-NTA agarose column. Previous results of chemical crosslinking showed that TetR6620 can form dimer but there is no evidence of UspA1171 capable of forming dimer. Nonetheless, with the presence of UspA1171 and BS3 crosslinker, there… Advisors/Committee Members: Wong, AOL, Tsang, JSH.

Subjects/Keywords: Genetic transcription - Regulation; Bacterial genetics; Transcription factors

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APA (6^th Edition):

Wang, S. (2016). Characterization of a universal stress protein UspA1171 of Burkholderia caribensis MBA4. (Masters Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/249195

Chicago Manual of Style (16^th Edition):

Wang, Shimeng. “Characterization of a universal stress protein UspA1171 of Burkholderia caribensis MBA4.” 2016. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. http://hdl.handle.net/10722/249195.

MLA Handbook (7^th Edition):

Wang, Shimeng. “Characterization of a universal stress protein UspA1171 of Burkholderia caribensis MBA4.” 2016. Web. 21 Jul 2019.

Vancouver:

Wang S. Characterization of a universal stress protein UspA1171 of Burkholderia caribensis MBA4. [Internet] [Masters thesis]. University of Hong Kong; 2016. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/10722/249195.

Council of Science Editors:

Wang S. Characterization of a universal stress protein UspA1171 of Burkholderia caribensis MBA4. [Masters Thesis]. University of Hong Kong; 2016. Available from: http://hdl.handle.net/10722/249195

Latrobe University

11. Do, Hai Thanh. Transcription factor binding sites identification using machine learning techniques.

Degree: PhD, 2011, Latrobe University

URL: http://hdl.handle.net/1959.9/527233

►

Thesis (Ph.D.) - La Trobe University, 2011

Submission note: "A thesis submitted in total fulfilment of the requirements for the degree of Doctor of Philosophy… (more)

Subjects/Keywords: Transcription factors.; Genetic transcription.; Gene expression.

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APA (6^th Edition):

Do, H. T. (2011). Transcription factor binding sites identification using machine learning techniques. (Doctoral Dissertation). Latrobe University. Retrieved from http://hdl.handle.net/1959.9/527233

Chicago Manual of Style (16^th Edition):

Do, Hai Thanh. “Transcription factor binding sites identification using machine learning techniques.” 2011. Doctoral Dissertation, Latrobe University. Accessed July 21, 2019. http://hdl.handle.net/1959.9/527233.

MLA Handbook (7^th Edition):

Do, Hai Thanh. “Transcription factor binding sites identification using machine learning techniques.” 2011. Web. 21 Jul 2019.

Vancouver:

Do HT. Transcription factor binding sites identification using machine learning techniques. [Internet] [Doctoral dissertation]. Latrobe University; 2011. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1959.9/527233.

Council of Science Editors:

Do HT. Transcription factor binding sites identification using machine learning techniques. [Doctoral Dissertation]. Latrobe University; 2011. Available from: http://hdl.handle.net/1959.9/527233

Portland State University

12. Sheffield, Kimberly Kay. Interplay of Transcription Factor E and Spt4/5 During Transcription Initiation in Pyrococcus furiosus.

Degree: MS(M.S.) in Biology, Biology, 2018, Portland State University

URL: https://pdxscholar.library.pdx.edu/open_access_etds/4444

► Transcription, the first step in gene expression, is a highly regulated process which relies on a multi-protein complex to occur. Among these proteins are… (more)

▼ Transcription, the first step in gene expression, is a highly regulated process which relies on a multi-protein complex to occur. Among these proteins are transcription factors, including initiation and elongation factors, which play differing roles in early and late stages of transcription. The mechanisms of transition from transcription initiation to elongation are not well understood in archaea, nor are the structures of the transcription factors involved. For transcription to occur in vitro, transcription factors TATA binding protein (TBP) and Transcription Factor B (TFB) are sufficient to allow RNA polymerase (RNAP) to synthesize RNA from template DNA. Another factor, Transcription Factor E (TFE), can also join the initiation complex and is likely to be essential in vivo. TFE is known to contribute to initiation by enhancing promoter opening, and while it has been shown to persist in elongation complexes, its role after initiation is unknown. Spt4/5, the archaeal homolog of the only universally conserved RNAP-associated factor, is known to join complexes in elongation steps and enhance processivity of the polymerase. However, if Spt4/5 joins pre-initiated complexes, it has been shown to inhibit transcription activity. The experiments in this thesis show that TFE and Spt4/5 participate in a crucial interchange at the upstream fork of the transcription bubble that helps define the timing of Spt4/5 binding. Using unnatural amino acid crosslinking techniques, the points of proximity between specific regions of these two factors and the template DNA have been mapped to identify possible sites of interaction. Competitive crosslinking assays indicate the exact timing of the shift in affinity between TFE and Spt4/5 for their shared binding site on RNAP. These data, combined with transcription assays, suggest a new role for TFE in preventing premature Spt4/5 binding, corresponding with a unique localized mobility within the winged helix of TFE. Advisors/Committee Members: Michael Bartlett.

Subjects/Keywords: Archaebacteria; Transcription factors; Genetic transcription; Biology

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APA (6^th Edition):

Sheffield, K. K. (2018). Interplay of Transcription Factor E and Spt4/5 During Transcription Initiation in Pyrococcus furiosus. (Masters Thesis). Portland State University. Retrieved from https://pdxscholar.library.pdx.edu/open_access_etds/4444

Chicago Manual of Style (16^th Edition):

Sheffield, Kimberly Kay. “Interplay of Transcription Factor E and Spt4/5 During Transcription Initiation in Pyrococcus furiosus.” 2018. Masters Thesis, Portland State University. Accessed July 21, 2019. https://pdxscholar.library.pdx.edu/open_access_etds/4444.

MLA Handbook (7^th Edition):

Sheffield, Kimberly Kay. “Interplay of Transcription Factor E and Spt4/5 During Transcription Initiation in Pyrococcus furiosus.” 2018. Web. 21 Jul 2019.

Vancouver:

Sheffield KK. Interplay of Transcription Factor E and Spt4/5 During Transcription Initiation in Pyrococcus furiosus. [Internet] [Masters thesis]. Portland State University; 2018. [cited 2019 Jul 21]. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/4444.

Council of Science Editors:

Sheffield KK. Interplay of Transcription Factor E and Spt4/5 During Transcription Initiation in Pyrococcus furiosus. [Masters Thesis]. Portland State University; 2018. Available from: https://pdxscholar.library.pdx.edu/open_access_etds/4444

University of Oklahoma

13. Zhao, Tao. Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS.

Degree: PhD, 2011, University of Oklahoma

URL: http://hdl.handle.net/11244/318596

► Animal neurons dynamically change their morphologies in response to steroid hormone signaling to adapt to changing environments. The molecular mechanisms underlying animal neuronal remodeling, however,… (more)

▼ Animal neurons dynamically change their morphologies in response to steroid hormone signaling to adapt to changing environments. The molecular mechanisms underlying animal neuronal remodeling, however, remain largely unknown. Metamorphosis is an important developmental stage in insects when crawling and feeding larvae transform into reproductive and flying adults. During this period, many insect larval neurons undergo dramatic morphological and functional alterations. These neuronal changes are regulated by a arthropod-specific steroid hormone, 20-hydroxyecdysone (ecdysone). Research on the metamorphic remodeling of insect neurons, has provided insights into the general neuronal remodeling process. During the early stage of metamorphosis, the larval neurons prune their projections and then grow out adult-specific neurites. A group of Drosophila melanogaster (fruit fly) neuroendocrine cells, the crustacean cardioactive peptide (CCAP) neurons, experiences metamorphic remodeling, and I used these neurons to dissect the molecular mechanisms controlling this process. The CCAP neurons mainly produce two neuropeptides, CCAP and bursicon, to control insect molting-related behaviors, ecdysis and wing expansion. Functional disruption of the CCAP neuron remodeling leads to defective wing expansion in adults. In a genetic screen, thousands of genes were mis- or overexpressed in the CCAP neurons. The genes that produced strong wing expansion defects were identified. Fourteen of the identified genes specifically inhibited the outgrowth of adult-specific neurites during metamorphic remodeling. One of these, split ends (spen) was selected to identify the molecular pathways affected by its overexpression. I performed a deficiency modifier screen to identify mutations that modify the outgrowth defects induced by spen. A mutation of Mbs, the gene encoding the Myosin binding subunit, moderately suppressed the outgrowth defects. Since Mbs negatively regulates myosin II activity, the results suggested that spen overexpressin suppressed myosin II activity. Another myosinmodulating signaling pathway, Rac1-PAK, was also tested to confirm the observations. The Rac1-PAK signaling pathway positively regulates myosin II function, and this pathway suppressed the neurite outgrowth defects induced by spen overexpression. Furthermore, down-regulation of spen activity strongly rescued the wing expansion and neurite growth defects resulting from disrupted Rac1-PAK signaling. These results strongly support a model in which spen functions antagonistically with myosin II to regulate neuronal outgrowth during metamorphosis. Advisors/Committee Members: Hewes, Randall S (advisor).

Subjects/Keywords: Neurons; Genetic transcription – Regulation; Transcription factors

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APA (6^th Edition):

Zhao, T. (2011). Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS. (Doctoral Dissertation). University of Oklahoma. Retrieved from http://hdl.handle.net/11244/318596

Chicago Manual of Style (16^th Edition):

Zhao, Tao. “Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS.” 2011. Doctoral Dissertation, University of Oklahoma. Accessed July 21, 2019. http://hdl.handle.net/11244/318596.

MLA Handbook (7^th Edition):

Zhao, Tao. “Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS.” 2011. Web. 21 Jul 2019.

Vancouver:

Zhao T. Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS. [Internet] [Doctoral dissertation]. University of Oklahoma; 2011. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/11244/318596.

Council of Science Editors:

Zhao T. Split ends (spen), A TRANSCRIPTIONAL REGULATOR, INHIBITS MYOSIN ACTIVITY TO REGULATE NEURONAL REMODELING DURING METAMORPHOSIS. [Doctoral Dissertation]. University of Oklahoma; 2011. Available from: http://hdl.handle.net/11244/318596

University of Utah

14. Seidel, Jeffrey John. Functions of the pointed domain within the ETS gene family;.

Degree: PhD, Oncological Sciences;, 2001, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/342/rec/554

► All members of the ets family of transcription factors conserve the DNA binding ETS domain that recognizes the core sequence 5’-GGA(A/T)-3’. Despite conserving this domain,… (more)

Subjects/Keywords: Transcription Factors

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APA (6^th Edition):

Seidel, J. J. (2001). Functions of the pointed domain within the ETS gene family;. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/342/rec/554

Chicago Manual of Style (16^th Edition):

Seidel, Jeffrey John. “Functions of the pointed domain within the ETS gene family;.” 2001. Doctoral Dissertation, University of Utah. Accessed July 21, 2019. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/342/rec/554.

MLA Handbook (7^th Edition):

Seidel, Jeffrey John. “Functions of the pointed domain within the ETS gene family;.” 2001. Web. 21 Jul 2019.

Vancouver:

Seidel JJ. Functions of the pointed domain within the ETS gene family;. [Internet] [Doctoral dissertation]. University of Utah; 2001. [cited 2019 Jul 21]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/342/rec/554.

Council of Science Editors:

Seidel JJ. Functions of the pointed domain within the ETS gene family;. [Doctoral Dissertation]. University of Utah; 2001. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/342/rec/554

University of Alberta

15. Strungaru, Marcela Hermina. Investigation of the role of PITX2 in ocular expression pathways and human disease.

Degree: PhD, Medical Sciences - Medical Genetics, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/v405sb16r

► The overall goal of my work has been to gain a better understanding of Axenfeld-Rieger Syndrome (ARS), a human autosomal dominantly inherited mal-development of the… (more)

▼ The overall goal of my work has been to gain a better understanding of Axenfeld-Rieger Syndrome (ARS), a human autosomal dominantly inherited mal-development of the anterior segment of the eye that is associated with glaucoma. By studying rare genetic causes of this complex disease we are gaining insight into the initial steps that ultimately lead to blindness. To achieve the goal of better understanding ARS, my research project had two parts. In the first part, I performed a retrospective clinical study in which I analyzed the glaucoma-related clinical presentation of ARS patients with FOXC1 and PITX2 defects. This study showed a good genotype-phenotype correlation which may be important for the physician in dealing with ARS patients. Patients with FOXC1 mutations had the mildest prognosis in glaucoma development, while patients with PITX2 defects and patients with FOXC1 duplication had a more severe prognosis in glaucoma development than patients with FOXC1 mutations. I tried to determine the best treatment for glaucoma in these patients. Unfortunately, in this study, current medical therapies did not successfully lower intraocular pressure or prevent progression of glaucoma in ARS patients with FOXC1 or PITX2 alterations. This clinical study also provided useful diagnostic criteria to identify the gene responsible for ARS. The second part of the project was to study the gene regulatory pathways of the PITX2 gene, mutations of which cause ARS. PITX2 is a transcription factor that regulates the expression of genes in the eye. The discovery of direct downstream targets of PITX2 is necessary for understanding the genetic mechanisms underlying complex, highly regulated processes such as development and underlying heritable human disorders. To find direct target genes of PITX2, I have used a recently developed method: the hormone receptor (HR)-inducible expression system for transcription factors coupled microarray analysis. The results obtained using this method have involved PITX2 in control of cellular stress. Recent investigations have suggested significant roles for cellular stress in glaucoma pathology. Understanding the control of these key aspects of cell function will have profound implications for understanding and treating the glaucoma that is the most clinically serious consequence of mutations of PITX2.

Subjects/Keywords: Glaucoma, Transcription Factors, Genes

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APA (6^th Edition):

Strungaru, M. H. (2010). Investigation of the role of PITX2 in ocular expression pathways and human disease. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/v405sb16r

Chicago Manual of Style (16^th Edition):

Strungaru, Marcela Hermina. “Investigation of the role of PITX2 in ocular expression pathways and human disease.” 2010. Doctoral Dissertation, University of Alberta. Accessed July 21, 2019. https://era.library.ualberta.ca/files/v405sb16r.

MLA Handbook (7^th Edition):

Strungaru, Marcela Hermina. “Investigation of the role of PITX2 in ocular expression pathways and human disease.” 2010. Web. 21 Jul 2019.

Vancouver:

Strungaru MH. Investigation of the role of PITX2 in ocular expression pathways and human disease. [Internet] [Doctoral dissertation]. University of Alberta; 2010. [cited 2019 Jul 21]. Available from: https://era.library.ualberta.ca/files/v405sb16r.

Council of Science Editors:

Strungaru MH. Investigation of the role of PITX2 in ocular expression pathways and human disease. [Doctoral Dissertation]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/v405sb16r

Texas A&M University

16. Hedrick, Erik Duane. Diindolylmethane Analogs as Novel NR4A1 Antagonists and as a Novel Class of Anticancer Agents and Sp Transcription Factors as Nononcogene Addiction Genes That Are Targets of ROS Inducing Agents.

Degree: 2016, Texas A&M University

URL: http://hdl.handle.net/1969.1/159116

► The orphan nuclear receptor 4A1 (NR4A1) and specificity protein (Sp) transcription factors (TFs) are both overexpressed in the majority of solid tumors. Our laboratory has… (more)

▼ The orphan nuclear receptor 4A1 (NR4A1) and specificity protein (Sp) transcription factors (TFs) are both overexpressed in the majority of solid tumors. Our laboratory has researched the molecular mechanisms of a novel class of 1,1-bis(3'-indolyl)-1-(p-substituted phenyl)methanes (C-DIMs) as NR4A1 antagonists and Sp proteins as non-oncogene addiction genes (NOA) that are targets of reactive oxygen species (ROS) inducing agents. Nr4A1 antagonists (DIM-C-pPhOH) (C-DIM 8) and (DIM-C-pPhCO2Me) (C-DIM 14) inhibited cancer cell proliferation, induced apoptosis, and inhibited migration. The NR4A1 antagonists inhibited constitutive and TGF?-induced migration in Triple Negative Breast Cancer (TNBC) cells. We also demonstrate that p38? is necessary and sufficient for TGF?-mediated migration and NR4A1 nuclear export in triple negative breast cancer (TNBC) which was attenuated with NR4A1 antagonists (C-DIMs), leptomycin B, and the p38 inhibitor SB202190. We also demonstrate that NR4A1 is essential for TGF?-induced EMT and NR4A1 antagonists promoted cytosolic sequestration of the transcription factor ?-catenin and its proteasome-dependent degradation in a time dependent manner. ?-catenin, along with TCF-3, TCF-4, and LEF-1 binds to TCF/LEF response elements in the NR4A1 promoter, regulating its expression. RNA interference (RNAi) demonstrates that Sp1, 3, and 4 TFs individually play a role in cancer cell growth, survival and migration/invasion in cancer cell lines. Individual knockdown of Sp1, Sp3, or Sp4, resulted in inhibition of cell growth, migration, and induction of apoptosis, with no compensation. Moreover, tumor growth in athymic nude mice bearing pancreatic cancer xenografts was significantly attenuated in cells depleted of Sp1, Sp3, and Sp4 in combination or Sp1 alone. Ingenuity Pathway Analysis (IPA) of changes in gene expression in Panc1 pancreatic cancer cells after individual knockdown of Sp TFs demonstrates that Sp1-, Sp3- and Sp4-regulated genes were associated with pro-oncogenic activity. C-DIMs are promising anticancer agents in NR4A1-overexpressing solid tumors and represent a novel class of mechanistic-based drugs that target TGF?/NR4A1-dependent inducible migration in TNBC. The functional and genomic results coupled with overexpression of Sp transcription factors in tumor vs. non-tumor tissues and decreased Sp1 expression with age indicate that Sp1, Sp3 and Sp4 are non-oncogene addiction (NOA) genes and are attractive drug targets for individual and combined cancer chemotherapies. Advisors/Committee Members: Safe, Stephen H (advisor), Burghardt, Robert C (committee member), Phillips, Timothy D (committee member), Tian, Yanan (committee member).

Subjects/Keywords: NR4A1; Sp transcription factors

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APA (6^th Edition):

Hedrick, E. D. (2016). Diindolylmethane Analogs as Novel NR4A1 Antagonists and as a Novel Class of Anticancer Agents and Sp Transcription Factors as Nononcogene Addiction Genes That Are Targets of ROS Inducing Agents. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/159116

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hedrick, Erik Duane. “Diindolylmethane Analogs as Novel NR4A1 Antagonists and as a Novel Class of Anticancer Agents and Sp Transcription Factors as Nononcogene Addiction Genes That Are Targets of ROS Inducing Agents.” 2016. Thesis, Texas A&M University. Accessed July 21, 2019. http://hdl.handle.net/1969.1/159116.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hedrick, Erik Duane. “Diindolylmethane Analogs as Novel NR4A1 Antagonists and as a Novel Class of Anticancer Agents and Sp Transcription Factors as Nononcogene Addiction Genes That Are Targets of ROS Inducing Agents.” 2016. Web. 21 Jul 2019.

Vancouver:

Hedrick ED. Diindolylmethane Analogs as Novel NR4A1 Antagonists and as a Novel Class of Anticancer Agents and Sp Transcription Factors as Nononcogene Addiction Genes That Are Targets of ROS Inducing Agents. [Internet] [Thesis]. Texas A&M University; 2016. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1969.1/159116.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hedrick ED. Diindolylmethane Analogs as Novel NR4A1 Antagonists and as a Novel Class of Anticancer Agents and Sp Transcription Factors as Nononcogene Addiction Genes That Are Targets of ROS Inducing Agents. [Thesis]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/159116

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

17. Malapi-Wight, Martha Maria. The Role of Cys2-His2 Zinc Finger Transcription Factors in Polyol Metabolism, Asexual Development and Fumonisin Biosynthesis in Fusarium verticillioides.

Degree: 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/149477

► The ascomycete Fusarium verticillioides (Sacc.) Nirenberg (teleomorph: Gibberella moniliformis Wineland) causes stalk and ear rots on maize worldwide. In addition to the economic losses due… (more)

▼ The ascomycete Fusarium verticillioides (Sacc.) Nirenberg (teleomorph: Gibberella moniliformis Wineland) causes stalk and ear rots on maize worldwide. In addition to the economic losses due to reduced yield, the fungus produces fumonisins on infected corn. One of the unanswered questions in mycotoxin research is how fungi perceive and respond to various extracellular stimuli and produce mycotoxins. To date, extensive research has been performed on important signaling pathways that regulate mycotoxin biosynthesis, but little is known about the downstream target genes, notably transcription factors (TFs). While the roles of TFs have shown to be critical in eukaryotic transcription regulation, only a few have been characterized in F. verticillioides. TFs with zinc fingers have been reported in all living organisms, and in fungal species, members of the Cys2-Hys2 (C2H2) zinc finger TF family are predicted to be involved in cell differentiation, carbon utilization, and development. Using the available genomic resources, I constructed a library of C2H2 TF deletion mutants, and identified SDA1, FvFLBC and CHT1 genes with a potential role in carbon utilization, development and fumonisin B1 (FB1) biosynthesis. The ?sda1 strain showed complete growth inhibition when using sorbitol as the sole carbon source and produced higher levels of FB1 when grown on corn kernels. In addition, the ?sda1 strain produced less number of conidia compared to the wild-type progenitor. Through gene complementation, I also demonstrated that F. verticillioides SDA1 and Trichoderma reesei ACE1 are functionally conserved. FvFLBC acts as a regulator of asexual development but not FB1 biosynthesis. I also discovered that the FvFlbC N-terminus is critical for conidia production. CHT1 is associated with asexual development, fumonisin biosynthesis and pigmentation. Characterization of key signal transduction pathways, and more importantly the function of SDA1, FvFLBC and CHT1, should facilitate the elucidation of the mechanisms and regulations of growth, development, and secondary metabolism in F. verticillioides. The outcome of this study may help us determine how to minimize F. verticillioides contamination of crops and the resulting mycotoxins, providing safer and higher value corn in the US and worldwide. Advisors/Committee Members: Shim, Won-Bo (advisor), He, Ping (committee member), Shaw, Brian D (committee member), Scholthof, Herman B (committee member).

Subjects/Keywords: Fusarium verticillioides; transcription factors

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APA (6^th Edition):

Malapi-Wight, M. M. (2013). The Role of Cys2-His2 Zinc Finger Transcription Factors in Polyol Metabolism, Asexual Development and Fumonisin Biosynthesis in Fusarium verticillioides. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/149477

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Malapi-Wight, Martha Maria. “The Role of Cys2-His2 Zinc Finger Transcription Factors in Polyol Metabolism, Asexual Development and Fumonisin Biosynthesis in Fusarium verticillioides.” 2013. Thesis, Texas A&M University. Accessed July 21, 2019. http://hdl.handle.net/1969.1/149477.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Malapi-Wight, Martha Maria. “The Role of Cys2-His2 Zinc Finger Transcription Factors in Polyol Metabolism, Asexual Development and Fumonisin Biosynthesis in Fusarium verticillioides.” 2013. Web. 21 Jul 2019.

Vancouver:

Malapi-Wight MM. The Role of Cys2-His2 Zinc Finger Transcription Factors in Polyol Metabolism, Asexual Development and Fumonisin Biosynthesis in Fusarium verticillioides. [Internet] [Thesis]. Texas A&M University; 2013. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1969.1/149477.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Malapi-Wight MM. The Role of Cys2-His2 Zinc Finger Transcription Factors in Polyol Metabolism, Asexual Development and Fumonisin Biosynthesis in Fusarium verticillioides. [Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/149477

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Oregon State University

18. Bredeweg, Erin L. Transcriptional networks controlled by the fatty acid regulators FAR-1 and FAR-2.

Degree: PhD, Molecular and Cellular Biology, 2014, Oregon State University

URL: http://hdl.handle.net/1957/46468

► Fungi are capable of growth on a wide variety of carbon sources, both living and dead. They can produce an arsenal of enzymes and transporters… (more)

▼ Fungi are capable of growth on a wide variety of carbon sources, both living and dead. They can produce an arsenal of enzymes and transporters for harvesting sugars, polysaccharides, amino acids, lipids and micronutrients from their environments [1]. Within the nucleus of a cell, transcription factors (TF) control whether genes will be transcribed, after which the transcripts can be translated into functional protein. TF contact with DNA can be influenced by nucleosomal occupancy, DNA binding affinity, and competition with other DNA binding proteins [2], [3]. Sequence specific DNA binding transcription factors associate with promoter sequences in order to tune core metabolic pathways in response to nutrient availability, for example N. crassa’s major nitrogen regulator NIT-2, [4], or in response to oxidative stress, the alternative oxidase regulator, AOD-2 [5]. Change in the relative abundance of proteins within the cell or "proteome" can have broad effects from redirection of metabolic flux via carbon and nitrogen use, production of enzymes for detoxification, and altered growth and development from the examples above. A survey of transcription factor binding influenced by light is underway in Neurospora crassa as part of the Neurospora Functional Genomics and Systems Biology (NcFGSB) program project funded by the NIH (P01GM). This work began by testing the link of FAR-1, or Fatty Acid Regulator -1 (NCU08000) to light regulation, but has continued toward investigation of how both FAR-1 and a second TF, Fatty Acid Regulator-2, or FAR-2 (NCU03643) influence central metabolism, oxidative stress response, and development. Transcription factor networks consist of describing TFs that bind to multiple genes and individual genes controlled by multiple regulators. Further, the "regulation of regulators" describes how the transcription of transcription factor genes is controlled. Chromatin immunoprecipitation, or 'ChIP' experiments show that a variety of factors are enriched at the same promoter region as can be seen by comparing multiple datasets [6], [7]. Transcriptional regulators may promote or inhibit one another from binding DNA, leading to a total regulation as the sum of TF activity. This complexity cannot be explained by single genetic experiments and study of a limited number of loci. Even in the event of TF association with specific promoter DNA as analyzed by ChIP, proximal binding of a transcriptional activator does not directly mean that transcript levels will increase, as we have seen with the identification of WC-2 binding sites [7]. I used a reverse genetics approach, assaying deletion mutants of selected loci, to determine the cellular effects of FAR-1 and FAR-2 transcriptional activity in different carbon sources. The tools of high throughput sequencing, and bioinformatics data analyses were combined with experiments to characterize phenotypes observed. Here I report (1) a collection of binding sites found in the Neurospora genome for FAR-1 and FAR-2 in sucrose, butyrate, and oleate, (2) changes in… Advisors/Committee Members: Freitag, Michael (advisor), Taylor, Barbara (committee member).

Subjects/Keywords: fatty acid; Transcription factors

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APA (6^th Edition):

Bredeweg, E. L. (2014). Transcriptional networks controlled by the fatty acid regulators FAR-1 and FAR-2. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/46468

Chicago Manual of Style (16^th Edition):

Bredeweg, Erin L. “Transcriptional networks controlled by the fatty acid regulators FAR-1 and FAR-2.” 2014. Doctoral Dissertation, Oregon State University. Accessed July 21, 2019. http://hdl.handle.net/1957/46468.

MLA Handbook (7^th Edition):

Bredeweg, Erin L. “Transcriptional networks controlled by the fatty acid regulators FAR-1 and FAR-2.” 2014. Web. 21 Jul 2019.

Vancouver:

Bredeweg EL. Transcriptional networks controlled by the fatty acid regulators FAR-1 and FAR-2. [Internet] [Doctoral dissertation]. Oregon State University; 2014. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/1957/46468.

Council of Science Editors:

Bredeweg EL. Transcriptional networks controlled by the fatty acid regulators FAR-1 and FAR-2. [Doctoral Dissertation]. Oregon State University; 2014. Available from: http://hdl.handle.net/1957/46468

University of Aberdeen

19. Ferguson, Laura A. The insulin promoter.

Degree: 2008, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=25965 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499108

► The aims of this thesis were to determine the relative contribution of Pdx-1, MafA and β2 to the human insulin promoter. Additionally, characterisation of the… (more)

Subjects/Keywords: 612.6; Insulin : Transcription factors

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APA (6^th Edition):

Ferguson, L. A. (2008). The insulin promoter. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=25965 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499108

Chicago Manual of Style (16^th Edition):

Ferguson, Laura A. “The insulin promoter.” 2008. Doctoral Dissertation, University of Aberdeen. Accessed July 21, 2019. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=25965 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499108.

MLA Handbook (7^th Edition):

Ferguson, Laura A. “The insulin promoter.” 2008. Web. 21 Jul 2019.

Vancouver:

Ferguson LA. The insulin promoter. [Internet] [Doctoral dissertation]. University of Aberdeen; 2008. [cited 2019 Jul 21]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=25965 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499108.

Council of Science Editors:

Ferguson LA. The insulin promoter. [Doctoral Dissertation]. University of Aberdeen; 2008. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=25965 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499108

University of Hong Kong

20. Kwok, Chun-ting, Davis. Expression and functions of FOXM1 in human embryonic stem cells.

Degree: M. Phil., 2014, University of Hong Kong

URL: Kwok, C. D. [郭俊廷]. (2014). Expression and functions of FOXM1 in human embryonic stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5388016 ; http://dx.doi.org/10.5353/th_b5388016 ; http://hdl.handle.net/10722/208629

► Human embryonic stem cells (hESCs) are characterized by unlimited proliferation (self-renewal), capability to differentiate into derivatives of all three germ layers (pluripotency), and abbreviated cell… (more)

▼ Human embryonic stem cells (hESCs) are characterized by unlimited proliferation (self-renewal), capability to differentiate into derivatives of all three germ layers (pluripotency), and abbreviated cell cycle structure. Despite tremendous efforts in identification of important regulators, the complicated molecular mechanisms and essential effectors underlying the distinctive features of hESCs have not yet been fully elucidated. Forkhead box transcription factor M1 (FOXM1) has been demonstrated to be critical for the maintenance of pluripotency in mouse embryonic stem cells (mESCs) and mouse embryonal carcinoma cells (mECCs). The present study hypothesized that FOXM1 is important to the self-renewing capacity and pluripotency of hESCs. The objectives of this study were to characterize FOXM1 expression in undifferentiated and differentiating hESCs, and to study the effect of perturbing FOXM1 expression on pluripotency and proliferation. Undifferentiated VAL3 analyzed by bivariate flow cytometric analysis revealed that FOXM1 expression was regulated in a cell cycle phase-dependent manner, with expression level increased from G1 through S phase, and eventually reached peak levels in G2/M phase. To study the subcellular localization of FOXM1 with respect to cell cycle progression, VAL3 cells were synchronized by nocodazole-mediated cell cycle block, followed by immunocytochemical analysis. The result indicated that FOXM1 underwent nuclear translocation at late-S and early-G2 phase of the cell cycle. When VAL3 spontaneously differentiated as embryoid bodies (EBs), the mRNA expression of FOXM1 displayed profound fluctuation over the differentiation process. Retinoic acid (RA) treatment induced rapid differentiation of VAL3, yet differential expression pattern of FOXM1 was observed for cells grown in different culture media. FOXM1 mRNA expression persisted in differentiating VAL3 cultured in mTeSR. By contrast, RA-driven differentiation of VAL3 cultured in conditioned medium was accompanied by transient depletion and resurgence of FOXM1 protein expression. Differentiation of VAL3 driven by Definitive Endoderm kit did not alter FOXM1 expression, whereas induced differentiation by Bone Morphogenic Protein 4 (BMP4) led to repression of FOXM1. The functional role of FOXM1 in hESCs was investigated with the use of siRNA. Transient knockdown of FOXM1in VAL3 did not induce substantial repression of pluripotent marker (OCT4, SOX2, NANOG) expression nor significant morphological change of colonies, despite upregulation of early differentiation marker SSEA-1. Intriguingly, FOXM1 depletion led to altered cell cycle progression and delay in G2 phase progression, possibly attributed to the downregulation of Cyclin B1 and Cdc25B. Also FOXM1 knockdown impaired VAL3 proliferation, yet no prominent defect in mitosis was observed. In conclusion, the present study reported for the first time the expression and functions of FOXM1 in undifferentiated hESCs. Upon differentiation, FOXM1 expression varied in cells committing to different…

Subjects/Keywords: Transcription factors; embryonic stem cells

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APA (6^th Edition):

Kwok, Chun-ting, D. (2014). Expression and functions of FOXM1 in human embryonic stem cells. (Masters Thesis). University of Hong Kong. Retrieved from Kwok, C. D. [郭俊廷]. (2014). Expression and functions of FOXM1 in human embryonic stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5388016 ; http://dx.doi.org/10.5353/th_b5388016 ; http://hdl.handle.net/10722/208629

Chicago Manual of Style (16^th Edition):

Kwok, Chun-ting, Davis. “Expression and functions of FOXM1 in human embryonic stem cells.” 2014. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. Kwok, C. D. [郭俊廷]. (2014). Expression and functions of FOXM1 in human embryonic stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5388016 ; http://dx.doi.org/10.5353/th_b5388016 ; http://hdl.handle.net/10722/208629.

MLA Handbook (7^th Edition):

Kwok, Chun-ting, Davis. “Expression and functions of FOXM1 in human embryonic stem cells.” 2014. Web. 21 Jul 2019.

Vancouver:

Kwok, Chun-ting D. Expression and functions of FOXM1 in human embryonic stem cells. [Internet] [Masters thesis]. University of Hong Kong; 2014. [cited 2019 Jul 21]. Available from: Kwok, C. D. [郭俊廷]. (2014). Expression and functions of FOXM1 in human embryonic stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5388016 ; http://dx.doi.org/10.5353/th_b5388016 ; http://hdl.handle.net/10722/208629.

Council of Science Editors:

Kwok, Chun-ting D. Expression and functions of FOXM1 in human embryonic stem cells. [Masters Thesis]. University of Hong Kong; 2014. Available from: Kwok, C. D. [郭俊廷]. (2014). Expression and functions of FOXM1 in human embryonic stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5388016 ; http://dx.doi.org/10.5353/th_b5388016 ; http://hdl.handle.net/10722/208629

Hong Kong University of Science and Technology

21. Poon, Lydia See Wing. Molecular basis of G[beta][gamma] signaling : dimer formation and interaction with effectors and Gα subunits.

Degree: 2009, Hong Kong University of Science and Technology

URL: https://doi.org/10.14711/thesis-b1040981 ; http://repository.ust.hk/ir/bitstream/1783.1-5968/1/th_redirect.html

► Heterotrimeric G proteins regulate multiple effectors of which some are mediated via the Gβγ dimers. There is evidence to suggest that the functions of Gβγ… (more)

▼ Heterotrimeric G proteins regulate multiple effectors of which some are mediated via the Gβγ dimers. There is evidence to suggest that the functions of Gβγ dimers are not shared by all possible permutations of Gβγ complexes. The aim of this research is to define the formation of distinct Gβγ dimers, their functional differences in activating downstream effectors such as phospholipase Cβ (PLCβ) isoforms, the molecular determinant of Gβγ formation and the dissociation of different G protein family members upon activation. Co-immunoprecipitation assays using COS7 cells transiently expressing 48 different combinations of Gβ(1-4) and Gγ1-5, 7-13) subunits showed that Gβ1 and Gβ4 could form dimers with all known Gγ subunits, whereas several dimers could not be observed for Gβ2 and Gβ3. All Gβ1γ and Gβ2γ dimers significantly stimulated PLCβ isoforms (PLCβ2 ≥ PLCβ3 > PLCβ1), but Gβ3γ and Gβ4γ dimers were poor activators of PLCβ1 and exhibited preference for PLCβ3 and PLCβ2, respectively. Mutation of certain residues in Gβ3 enhanced PLCβ2-activating functions when co-expressed with different Gγ subunits, while the corresponding stimulation on PLCβ3 was not altered. All these results show that the exact composition of a Gβγ dimer can determine its selectivity for activating PLCβ isoforms, and certain residues in Gβ3 may account for the preferential stimulation of PLCβ3 by Gβ3γ dimers. Apart from the N-terminal α helix and blades 5 – 7 of Gβ subunits, the region of blades 1 – 4 also play a minor but significant role in Gβγ dimer formation. Furthermore, different from the classical model of G protein activation upon receptor-mediated activation, some activated Gα subunits, including Gαq, Gα11, Gα14, Gα16, Gαz, Gαt1, Gαt2, Gαs, Gαolf, Gα12 and Gα13, may remain associate with Gβγ dimer upon G protein activation, indicating that a new model of G protein activation mechanism is required for replacement of the classical model in which G protein activation is always coupled with subunit dissociation.

Subjects/Keywords: G proteins; Transcription factors; Dimers

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APA (6^th Edition):

Poon, L. S. W. (2009). Molecular basis of G[beta][gamma] signaling : dimer formation and interaction with effectors and Gα subunits. (Thesis). Hong Kong University of Science and Technology. Retrieved from https://doi.org/10.14711/thesis-b1040981 ; http://repository.ust.hk/ir/bitstream/1783.1-5968/1/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 (16^th Edition):

Poon, Lydia See Wing. “Molecular basis of G[beta][gamma] signaling : dimer formation and interaction with effectors and Gα subunits.” 2009. Thesis, Hong Kong University of Science and Technology. Accessed July 21, 2019. https://doi.org/10.14711/thesis-b1040981 ; http://repository.ust.hk/ir/bitstream/1783.1-5968/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Poon, Lydia See Wing. “Molecular basis of G[beta][gamma] signaling : dimer formation and interaction with effectors and Gα subunits.” 2009. Web. 21 Jul 2019.

Vancouver:

Poon LSW. Molecular basis of G[beta][gamma] signaling : dimer formation and interaction with effectors and Gα subunits. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2009. [cited 2019 Jul 21]. Available from: https://doi.org/10.14711/thesis-b1040981 ; http://repository.ust.hk/ir/bitstream/1783.1-5968/1/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:

Poon LSW. Molecular basis of G[beta][gamma] signaling : dimer formation and interaction with effectors and Gα subunits. [Thesis]. Hong Kong University of Science and Technology; 2009. Available from: https://doi.org/10.14711/thesis-b1040981 ; http://repository.ust.hk/ir/bitstream/1783.1-5968/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

22. Jia, Huiqiang. Dynamics of mitochondrial RNA polymerase transcription elongation in the presence of DNA damage and the effect of transcription factors.

Degree: 2016, Hong Kong University of Science and Technology

URL: https://doi.org/10.14711/thesis-b1626253 ; http://repository.ust.hk/ir/bitstream/1783.1-87117/1/th_redirect.html

► As the first step of gene expression, accurate transcription is essential to keep normal translation and the functions of proteins. Human mitochondrial RNA polymerase (POLRMT,… (more)

Subjects/Keywords: RNA polymerases; Transcription factors; Mitochondria

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APA (6^th Edition):

Jia, H. (2016). Dynamics of mitochondrial RNA polymerase transcription elongation in the presence of DNA damage and the effect of transcription factors. (Thesis). Hong Kong University of Science and Technology. Retrieved from https://doi.org/10.14711/thesis-b1626253 ; http://repository.ust.hk/ir/bitstream/1783.1-87117/1/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 (16^th Edition):

Jia, Huiqiang. “Dynamics of mitochondrial RNA polymerase transcription elongation in the presence of DNA damage and the effect of transcription factors.” 2016. Thesis, Hong Kong University of Science and Technology. Accessed July 21, 2019. https://doi.org/10.14711/thesis-b1626253 ; http://repository.ust.hk/ir/bitstream/1783.1-87117/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jia, Huiqiang. “Dynamics of mitochondrial RNA polymerase transcription elongation in the presence of DNA damage and the effect of transcription factors.” 2016. Web. 21 Jul 2019.

Vancouver:

Jia H. Dynamics of mitochondrial RNA polymerase transcription elongation in the presence of DNA damage and the effect of transcription factors. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2016. [cited 2019 Jul 21]. Available from: https://doi.org/10.14711/thesis-b1626253 ; http://repository.ust.hk/ir/bitstream/1783.1-87117/1/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:

Jia H. Dynamics of mitochondrial RNA polymerase transcription elongation in the presence of DNA damage and the effect of transcription factors. [Thesis]. Hong Kong University of Science and Technology; 2016. Available from: https://doi.org/10.14711/thesis-b1626253 ; http://repository.ust.hk/ir/bitstream/1783.1-87117/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Hong Kong

23. Chen, Zheyi. Down-regulation of the expression of Pax6 through Aβ insults in Alzheimer’s disease cell model.

Degree: Master of Medical Sciences, 2017, University of Hong Kong

URL: http://hdl.handle.net/10722/252449

►

Alzheimer’s disease (AD) is one of the major neurodegenerative diseases that seriously affect the central nervous system (CNS). It features progressive loss of memory, linguistic… (more)

▼

Alzheimer’s disease (AD) is one of the major neurodegenerative diseases that seriously affect the central nervous system (CNS). It features progressive loss of memory, linguistic competence, mobility and coordination, as well as great change in personality. Due to its dynamic disease progression, there are no perfect biomarkers till now. As aging becomes a worldwide issue, a quality life of the senile people calls for early diagnosis, efficient cure and better prognosis of this distracting disease. Though scientists are still struggling in the marsh, trying to figure out any clues to explain the relationship between Alzheimer’s disease and amyloid/tau hypothesis, microglia steps onto the stage for its important role as phagocytic cells in the CNS. Now it’s almost a common sense that neurodegeneration diseases are closely related with dysfunctional clearance of dead cells and neuroinflammation. Thus, the receptors expressed by microglia become hot spot. In the present study, I firstly localized the intracellular expression of Pax6 and found out that in the natural case it was universally distributed with a higher expression level in the nucleus. But when overexpressed, it seemed that the protein products intended to retain within the nucleus. Then, I constructed one Pax6 knock-down stable cell line and one Pax6 transiently overexpressed cell line and the expression levels of five target genes (TREM2, GAS6, CD36, ANXA1 and MFG-E8) screened from previous studies were measured using qRT-PCR (quantitative reverse transcription polymerase chain reaction) respectively. The data showed a significant correspondence between Pax6 and TREM2 which indicated a probable intermediate regulatory role of Pax6 on TREM2. These results confirmed Pax6 to be a DNA-binding transcription factor and extended the mechanism behind its deteriorative role as it could down-regulate the expression of TREM2, which was recognized as a positive player in AD pathology. Furthermore, the result raised the possibilities that Pax6 could be an effective therapeutic target, and the potential of TREM2 as a novel biomarker.

published_or_final_version

Biomedical Sciences

Master

Master of Medical Sciences

Subjects/Keywords: Transcription factors; Alzheimer's disease

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chen, Z. (2017). Down-regulation of the expression of Pax6 through Aβ insults in Alzheimer’s disease cell model. (Masters Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/252449

Chicago Manual of Style (16^th Edition):

Chen, Zheyi. “Down-regulation of the expression of Pax6 through Aβ insults in Alzheimer’s disease cell model.” 2017. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. http://hdl.handle.net/10722/252449.

MLA Handbook (7^th Edition):

Chen, Zheyi. “Down-regulation of the expression of Pax6 through Aβ insults in Alzheimer’s disease cell model.” 2017. Web. 21 Jul 2019.

Vancouver:

Chen Z. Down-regulation of the expression of Pax6 through Aβ insults in Alzheimer’s disease cell model. [Internet] [Masters thesis]. University of Hong Kong; 2017. [cited 2019 Jul 21]. Available from: http://hdl.handle.net/10722/252449.

Council of Science Editors:

Chen Z. Down-regulation of the expression of Pax6 through Aβ insults in Alzheimer’s disease cell model. [Masters Thesis]. University of Hong Kong; 2017. Available from: http://hdl.handle.net/10722/252449

University of Hong Kong

24. 許文寧; Hui, Man-ning. Investigating the role of SOX9 in human neural stem cells.

Degree: M. Phil., 2013, University of Hong Kong

URL: Hui, M. [許文寧]. (2013). Investigating the role of SOX9 in human neural stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5108699 ; http://dx.doi.org/10.5353/th_b5108699 ; http://hdl.handle.net/10722/193481

►

Neural stem cells (NSCs) exist in both embryonic and adult neural tissues and are characterized by their self-renewal capacity and multipotency that contribute to the… (more)

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Neural stem cells (NSCs) exist in both embryonic and adult neural tissues and are characterized by their self-renewal capacity and multipotency that contribute to the generation of three major cell types in the vertebrate central nervous system (CNS):neurons, oligodendrocytes and astrocytes. The tremendous therapeutic potential of NSCs to treat the neurodegenerative diseases and repair brain injuries has provoked intensive study in the molecular regulation of their induction, maintenance and differentiation. Previous study reported that Sox9, a member of high-mobility-group(HMG) containing SoxE transcription factors family, plays important roles in regulating the formation and maintenance of NSCs in both mouse and chick CNS, as well as the cell fate switch between neuronal and glial. Whether it plays similar roles in human NSCs (hNSCs)is still unknown. My RT-qPCR analysis showed that SOX9is expressed at a basal level in human embryonic stem cells (hESCs) and up-regulated upon commitment into neural lineage and maintained at a high level in hESCs-derived hNSCs. I therefore hypothesized that SOX9 might also be involved in the induction, maintenance and differentiation of hNSCs. To test this, two stable hESC lines(HES2)were generated with each constitutively expressing short hairpin RNA (shRNA) against SOX9andGL2 Luciferase (Luc, as control) respectively. Upon neural induction, SOX9-knock-down(KD) hESCs were able to commit neural lineage and differentiate into NSCs/neurospheres (NSPs), however, these NSCs exhibited reduced multipotency and glial marker (GALC, CD44) expressions but enhanced self-renewal compared to the shLuc NSCs. Hence, SOX9 is required for both the induction and maintenance of multipotent hNSCs. Strikingly, extensive TUJ1+ neurites and advance groupings of these neurites into bundles were observed in SOX9-KD NSPs after three days and seven days neuronal differentiation respectively, suggesting premature neurogenesis as a result of SOX9 ablation. In addition, RT-qPCR analysis revealed down-regulated expression of NSC marker HES1but induced proneural basic helix-loop-helix transcription factor MASH1in shSOX9-1208 NSCs. The inhibitory role of HES1 on the expression and functions of MASH1 has been reported to be essential for the timely generation of neurons. Hence, ablation of SOX9 is likely to relieve the inhibition on MASH1activity via down-regulated HES1expression and leads to early neuronal differentiation. Expression of the potent neurite blocker NG2 was also found to be reduced in SOX9-KD NSCs which may explain the extensive neurite network observed. Altogether, similar to previous studies in mouse NSCs, SOX9 is also required for the induction and maintenance of hNSCs. However, this study further reveals a putative novel role of SOX9 in preventing premature neuronal differentiation by regulating the expressions of HES1 to counteract MASH1 function and NG2 to control neurite outgrowth.

published_or_final_version

Biochemistry

Master

Master of Philosophy

Subjects/Keywords: Neural stem cells; Transcription factors

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APA (6^th Edition):

許文寧; Hui, M. (2013). Investigating the role of SOX9 in human neural stem cells. (Masters Thesis). University of Hong Kong. Retrieved from Hui, M. [許文寧]. (2013). Investigating the role of SOX9 in human neural stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5108699 ; http://dx.doi.org/10.5353/th_b5108699 ; http://hdl.handle.net/10722/193481

Chicago Manual of Style (16^th Edition):

許文寧; Hui, Man-ning. “Investigating the role of SOX9 in human neural stem cells.” 2013. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. Hui, M. [許文寧]. (2013). Investigating the role of SOX9 in human neural stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5108699 ; http://dx.doi.org/10.5353/th_b5108699 ; http://hdl.handle.net/10722/193481.

MLA Handbook (7^th Edition):

許文寧; Hui, Man-ning. “Investigating the role of SOX9 in human neural stem cells.” 2013. Web. 21 Jul 2019.

Vancouver:

許文寧; Hui M. Investigating the role of SOX9 in human neural stem cells. [Internet] [Masters thesis]. University of Hong Kong; 2013. [cited 2019 Jul 21]. Available from: Hui, M. [許文寧]. (2013). Investigating the role of SOX9 in human neural stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5108699 ; http://dx.doi.org/10.5353/th_b5108699 ; http://hdl.handle.net/10722/193481.

Council of Science Editors:

許文寧; Hui M. Investigating the role of SOX9 in human neural stem cells. [Masters Thesis]. University of Hong Kong; 2013. Available from: Hui, M. [許文寧]. (2013). Investigating the role of SOX9 in human neural stem cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5108699 ; http://dx.doi.org/10.5353/th_b5108699 ; http://hdl.handle.net/10722/193481

University of Hong Kong

25. Tse, Yuen-yu, Belinda. Expression of FOXP1 in breast cancer.

Degree: Master of Medical Sciences, 2013, University of Hong Kong

URL: Tse, Y. B. [謝宛余]. (2013). Expression of FOXP1 in breast cancer. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091489 ; http://dx.doi.org/10.5353/th_b5091489 ; http://hdl.handle.net/10722/193527

► Objectives: Forkhead box protein P1 (FOXP1) is a transcription factor, and a member of the P-subfamily of forkhead box transcription factor and regulate transcription of… (more)

▼ Objectives: Forkhead box protein P1 (FOXP1) is a transcription factor, and a member of the P-subfamily of forkhead box transcription factor and regulate transcription of a subset of genes that involved in various cellular events. It plays a critical role in regulating cell growth and proliferation, differentiation, embryogenesis, adult tissue homeostasis, and possibly tumorigenesis. Predominant nuclear localisation of FOXP1 protein is commonly expressed at low level in normal tissues and upregulated in proliferative cells. Studies have demonstrated that the loss of FOXP1 expression and cytoplasmic mis-localisation is significantly associated with various malignant cancers, including breast cancer. FOXP1 can act either as a tumor suppressor or as an oncogenic protein in cell-type specific functions. It has been shown to be a co-regulator of estrogen receptor alpha and can modify a specific subset of forkhead box transcription factor class O (FOXO)-target genes. We hypothesise that there is association between FOXP1 expression and patient survival, and explore the potential role of FOXP1 expression as a prognostic marker in breast cancer. Methods: One hundred and twenty breast cancer samples in tissue microarray blocks were examined for FOXP1 expression by immuno-histochemistry. Nuclear and cytoplasmic FOXP1 expression patterns were analysed with clinico-pathological parameters. Statistical analysis was performed using SPSS software to determine the correlation between FOXP1 expression and clinico-pathological parameters. The correlation between subcellular FOXP1 expression and survival was evaluated by COX regression analysis. Results: Nuclear or cytoplasmic FOXP1 expression showed no association with clinico-pathological parameters. However, our results showed that there was significant association with estrogen receptor and progesterone receptor when nuclear and cytoplasmic scores were combined as total FOXP1 score (p=0.022 and p=0.028 respectively). In univariate analysis, high nuclear and cytoplasmic FOXP1 expression had no significant correlation with poor survival, while high total FOXP1 expression was associated with poor overall and disease-specific survival (p=0.045). Tumor stage and lymph-node involvement were significantly related to poorer overall and disease-specific survival, while other clinico-pathological parameters did not. In breast cancer with advanced tumor grade and lymph-node involvement, overall and disease-specific survival are significantly associated with high FOXP1 expression (p=0.041 and p=0.015 respectively). Conclusion: Unlike previous reports, our findings show that increased nuclear and cytoplasmic FOXP1 expression were both observed and high total FOXP1 expression was associated with poorer survival, particularly in cases of advance tumor grade and with lymph node metastases. These finding are supported by a recent report that showed that FOXP1 can up-regulate its own expression by binding to the promoter of FOXP1 and promote cell survival of breast cancer cells by suppressing…

Subjects/Keywords: Transcription factors; Breast - Cancer

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APA (6^th Edition):

Tse, Yuen-yu, B. (2013). Expression of FOXP1 in breast cancer. (Masters Thesis). University of Hong Kong. Retrieved from Tse, Y. B. [謝宛余]. (2013). Expression of FOXP1 in breast cancer. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091489 ; http://dx.doi.org/10.5353/th_b5091489 ; http://hdl.handle.net/10722/193527

Chicago Manual of Style (16^th Edition):

Tse, Yuen-yu, Belinda. “Expression of FOXP1 in breast cancer.” 2013. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. Tse, Y. B. [謝宛余]. (2013). Expression of FOXP1 in breast cancer. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091489 ; http://dx.doi.org/10.5353/th_b5091489 ; http://hdl.handle.net/10722/193527.

MLA Handbook (7^th Edition):

Tse, Yuen-yu, Belinda. “Expression of FOXP1 in breast cancer.” 2013. Web. 21 Jul 2019.

Vancouver:

Tse, Yuen-yu B. Expression of FOXP1 in breast cancer. [Internet] [Masters thesis]. University of Hong Kong; 2013. [cited 2019 Jul 21]. Available from: Tse, Y. B. [謝宛余]. (2013). Expression of FOXP1 in breast cancer. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091489 ; http://dx.doi.org/10.5353/th_b5091489 ; http://hdl.handle.net/10722/193527.

Council of Science Editors:

Tse, Yuen-yu B. Expression of FOXP1 in breast cancer. [Masters Thesis]. University of Hong Kong; 2013. Available from: Tse, Y. B. [謝宛余]. (2013). Expression of FOXP1 in breast cancer. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091489 ; http://dx.doi.org/10.5353/th_b5091489 ; http://hdl.handle.net/10722/193527

University of Hong Kong

26. Mak, Wing-nga. Role of Sox9 in cancer stemness of hepatocellular carcinoma.

Degree: M. Phil., 2015, University of Hong Kong

URL: Mak, W. [麥詠雅]. (2015). Role of Sox9 in cancer stemness of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5689268. ; http://dx.doi.org/10.5353/th_b5689268 ; http://hdl.handle.net/10722/235793

► In spite of the great effort invested in research and invention of advanced therapeutic treatments, HCC remains one of the deadliest cancers worldwide with high… (more)

▼ In spite of the great effort invested in research and invention of advanced therapeutic treatments, HCC remains one of the deadliest cancers worldwide with high relapse rate, chemoresistance and metastatic potential. It is suggested that the existence of cancer stem cells (CSCs) may account for the aggressive nature of HCC and the failure of current treatments. The hypothesis of CSC proposed a hierarchy in the heterogeneous tumor bulk. Only a small subset of malignant cells has the capability to initiate tumor formation and bears stem cell-like features such as self-renewal and chemoresistance. For this reason targeting CSC may underlie novel therapeutic strategies for eliminating HCC. Accumulating evidence suggests that dysregulation of development-related genes may promote carcinogenesis. As a transcription factor of the sex-determining region Y-related high-mobility-goup Box (Sox) family, Sox9 participates in embryogenesis and stem/progenitor cell maintenance. It was demonstrated to be upregulated and serve oncogenic functions in various human malignancies including HCC. However, its in vivo function was not validated in primary liver cancer. In addition, Sox9 expression has been observed in putative hepatic progenitor cells and contributes to self-renewal of these adult progenitors. Therefore, we hypothesized that Sox9 may promote the acquirement of stemness properties in human HCC. In the current project, we first investigated the clinical significance of Sox9 in human HCC samples followed by in vitro and in vivo functional roles of this Sox protein in human HCC cells. Our findings presented that Sox9 was upregulated in human HCC tumor tissues when compared to their corresponding non-tumorous counterparts. Such upregulation was correlated with poorer cellular differentiation and presence of venous invasion, implying an oncogenic role of Sox9 in HCC aggressiveness and metastasis. Sox9 was also found co-expressed with hepatic progenitor marker CK19 in some of human HCC tissues, suggesting that Sox9 may promote stemness traits in HCC. Using shRNA stable knockdown approach, our in vitro studies presented downregulation of a panel of stem cell-related genes and attenuation of cell proliferation upon knocking down Sox9. More importantly, we have provided the first piece of evidence that silencing Sox9 could greatly inhibit in vitro self-renewal and in vivo tumor initiation and progression in HCC. Furthermore, our functional studies demonstrated that knockdown of Sox9 could led to suppression of in vitro migratory ability and invasiveness as well as epithelial-mesenchymal transition. These findings further supported the notion that Sox9 may contribute to the augmentation of cancer stemness and metastatic potential in HCC. In conclusion, this study presented upregulation of Sox9 in human HCC samples and provided evidence of the oncogenic role of Sox9 in promoting cancer stemness in HCC. It implied that targeting this Sox protein may present a new therapeutic strategy that aids elimination of the tumor-initiating…

Subjects/Keywords: Liver - Cancer; Transcription factors

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APA (6^th Edition):

Mak, W. (2015). Role of Sox9 in cancer stemness of hepatocellular carcinoma. (Masters Thesis). University of Hong Kong. Retrieved from Mak, W. [麥詠雅]. (2015). Role of Sox9 in cancer stemness of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5689268. ; http://dx.doi.org/10.5353/th_b5689268 ; http://hdl.handle.net/10722/235793

Chicago Manual of Style (16^th Edition):

Mak, Wing-nga. “Role of Sox9 in cancer stemness of hepatocellular carcinoma.” 2015. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. Mak, W. [麥詠雅]. (2015). Role of Sox9 in cancer stemness of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5689268. ; http://dx.doi.org/10.5353/th_b5689268 ; http://hdl.handle.net/10722/235793.

MLA Handbook (7^th Edition):

Mak, Wing-nga. “Role of Sox9 in cancer stemness of hepatocellular carcinoma.” 2015. Web. 21 Jul 2019.

Vancouver:

Mak W. Role of Sox9 in cancer stemness of hepatocellular carcinoma. [Internet] [Masters thesis]. University of Hong Kong; 2015. [cited 2019 Jul 21]. Available from: Mak, W. [麥詠雅]. (2015). Role of Sox9 in cancer stemness of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5689268. ; http://dx.doi.org/10.5353/th_b5689268 ; http://hdl.handle.net/10722/235793.

Council of Science Editors:

Mak W. Role of Sox9 in cancer stemness of hepatocellular carcinoma. [Masters Thesis]. University of Hong Kong; 2015. Available from: Mak, W. [麥詠雅]. (2015). Role of Sox9 in cancer stemness of hepatocellular carcinoma. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5689268. ; http://dx.doi.org/10.5353/th_b5689268 ; http://hdl.handle.net/10722/235793

University of Hong Kong

27. Tsang, Kwong-shing. FBI-1 and AMPK in choriocarcinoma cells.

Degree: Master of Medical Sciences, 2015, University of Hong Kong

URL: Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489

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Choriocarcinoma is a rare and highly aggressive tumorwhich belongs to the gestational trophoblastic diseases (GTD). It can be originated from either gestational or non-gestational origins.… (more)

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Choriocarcinoma is a rare and highly aggressive tumorwhich belongs to the gestational trophoblastic diseases (GTD). It can be originated from either gestational or non-gestational origins. Choriocarcinoma is characterized by biphasic pattern and is composed of a mixed population of mononuclear cytotrophoblasts and multinucleated syncytotrophoblasts. Because of its low prevalence, information on the biology of choriocarcinoma is still insufficient. FBI-1 is an oncogenic transcription factor that is found to be overexpressed in various cancers. In our previous study, overexpression of FBI-1 in gestational choriocarcinoma cell lines,JEG-3 and JAR, were found. FBI-1 affects cell survival through regulating apoptosis and modulating cell motility in choriocarcinoma cells. However, the underlying mechanisms on how FBI-1affectscellular functions is largely unknown. AMPK is a master regulator in metabolic pathways and helps cells to maintain energy homeostasis in response to stressful conditions. Dysregulation on AMPK upsets the balance in metabolism that may play a role in the pathogenesis of cancers. Besides, AMPK is strongly associated with Warburg effect which is considered as a hallmark of cancer. In this study, we aim to investigate the relation between FBI-1 and AMPK in choriocarcinoma. Normal trophoblast cell lines HTR-8/SVneo and TEV-1as well as choriocarcinoma cell lines JAR, BeWo and JEG-3 were used. Levels of mRNA and protein expressions were evaluated by qRT-PCR and western blot respectively. In choriocarcinoma cell lines, relative lower levels of both AMPKα1 andα2 mRNA and protein were demonstrated when compared with the normal trophoblast cells lines. After knock down of FBI-1 in choriocarcinoma cell lines,JEG-3 and JAR, the expression of AMPK α1 but not theα2 subunit was suppressed. The expressions of a panel of glycolysis-related genes, including hexokinase II (HK2), phosphoglycerate kinase 1 (PGK1), lactate dehydrogenase A (LDHA), pyruvate kinase muscle isozymeM2 (PKM2), aldolase C (ALDOC) and glucose transporter 1(GLUT1), were examined in this study. It was found that the expressions of most of these genes were unaffected. ALDOC mRNA and HK2 protein expression was found to decrease in choriocarcinoma cells with FBI-1 knockdown, suggesting that glycolytic pathway was affected by FBI-1. These results tend to indicate that AMPK may cooperate with FBI-1 in choriocarcinoma cells to gain survival advantages through modulation of glycolysis although further study is needed.

published_or_final_version

Pathology

Master

Master of Medical Sciences

Subjects/Keywords: Protein kinases; Transcription factors; Choriocarcinoma

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APA (6^th Edition):

Tsang, K. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Masters Thesis). University of Hong Kong. Retrieved from Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489

Chicago Manual of Style (16^th Edition):

Tsang, Kwong-shing. “FBI-1 and AMPK in choriocarcinoma cells.” 2015. Masters Thesis, University of Hong Kong. Accessed July 21, 2019. Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489.

MLA Handbook (7^th Edition):

Tsang, Kwong-shing. “FBI-1 and AMPK in choriocarcinoma cells.” 2015. Web. 21 Jul 2019.

Vancouver:

Tsang K. FBI-1 and AMPK in choriocarcinoma cells. [Internet] [Masters thesis]. University of Hong Kong; 2015. [cited 2019 Jul 21]. Available from: Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489.

Council of Science Editors:

Tsang K. FBI-1 and AMPK in choriocarcinoma cells. [Masters Thesis]. University of Hong Kong; 2015. Available from: Tsang, K. [曾廣成]. (2015). FBI-1 and AMPK in choriocarcinoma cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659705 ; http://hdl.handle.net/10722/221489

University of Hong Kong

28. 趙楓; Zhao, Fung. Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance.

Degree: PhD, 2014, University of Hong Kong

URL: Zhao, F. [趙楓]. (2014). Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5312325 ; http://dx.doi.org/10.5353/th_b5312325 ; http://hdl.handle.net/10722/211053

► Ovarian carcinoma is the most lethal gynecological malignancy. The high relapse and mortality rates are attributable to late diagnosis and development of drug resistance. Identifying… (more)

▼ Ovarian carcinoma is the most lethal gynecological malignancy. The high relapse and mortality rates are attributable to late diagnosis and development of drug resistance. Identifying novel prognostic and therapeutic targets for ovarian carcinoma is crucial for improving patients' long-term survival rate. Forkhead box protein M1 (FOXM1), which is a widely studied member of the FOX superfamily of proteins, participates in cell proliferation and apoptosis affecting the developmental function of many organs. Recently, there has been emerging evidence supporting the biological significance of FOXM1 in carcinogenesis. Overexpression of FOXM1 has been reported in multiple human malignancies including primary breast cancer, lung cancer, prostate cancer, etc. However, whether FOXM1 participates in the development of ovarian cancer, with emphasis on the association with clinicopathological parameters and chemoresistance, remains unknown. This study aims at elucidating the functional role of FOXM1 in the tumorigenesis of ovarian cancer. Immunohistochemical study showed higher nuclear FOXM1 expression was significantly associated with advanced stages of ovarian cancer (P=0.035). Though not reaching statistical significance, FOXM1 overexpression displayed association with serous histologic subtype, high grade cancers (poor differentiation) and chemoresistance. Patients with a low FOXM1 level had a significantly longer overall (P=0.019) and disease-free survival (P=0.014) than those with high FOXM1 expression. Multivariate progression analysis established high expression of FOXM1, advanced cancer stages and poor histological differentiation (high grade) as independent prognostic factors for short overall and disease-free survival. Consistently, in vitro Transwell assays demonstrated transient knockdown of FOXM1 was capable of reducing SKOV-3 migration and invasion. Furthermore, paclitaxel treatment down-regulated FOXM1 expression in the sensitive cell line but not the resistant one. Immunofluorescence and flow cytometric analyses demonstrated FOXM1 knockdown could enhance paclitaxel-mediated mitotic catastrophe in ovarian cancer cells. Recent attention has been drawn to the oncogenic roles of kinesin-like protein KIF2C and p21-activated kinase 4 (PAK4) in human cancers. Interestingly, the expressions of KIF2C and PAK4 altered in a similar pattern to FOXM1 expression upon paclitaxel treatment by displaying down-regulation only in the paclitaxel sensitive cell line but not the resistant one. FOXM1 silencing, qPCR, luciferase reporter assay and chromatin immunoprecipitation confirmed KIF2C and PAK4 to be novel transcriptional targets of FOXM1. Clonogenic assay showed KIF2C knockdown could re-sensitize resistant cell line to paclitaxel treatment. Flow cytometry demonstrated KIF2C silencing was able to increase the number of cells blocked at G2/M cell cycle phase in sensitive cell line and raise the number of apoptotic cells in resistant cell line. Up-regulations of miR-590 and miR-370 were also observed in a panel of drug…

Subjects/Keywords: Transcription factors; Ovaries - Cancer

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APA (6^th Edition):

趙楓; Zhao, F. (2014). Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. (Doctoral Dissertation). University of Hong Kong. Retrieved from Zhao, F. [趙楓]. (2014). Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5312325 ; http://dx.doi.org/10.5353/th_b5312325 ; http://hdl.handle.net/10722/211053

Chicago Manual of Style (16^th Edition):

趙楓; Zhao, Fung. “Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed July 21, 2019. Zhao, F. [趙楓]. (2014). Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5312325 ; http://dx.doi.org/10.5353/th_b5312325 ; http://hdl.handle.net/10722/211053.

MLA Handbook (7^th Edition):

趙楓; Zhao, Fung. “Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance.” 2014. Web. 21 Jul 2019.

Vancouver:

趙楓; Zhao F. Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2019 Jul 21]. Available from: Zhao, F. [趙楓]. (2014). Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5312325 ; http://dx.doi.org/10.5353/th_b5312325 ; http://hdl.handle.net/10722/211053.

Council of Science Editors:

趙楓; Zhao F. Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Zhao, F. [趙楓]. (2014). Role of FOXM1 in ovarian cancer tumorigenesis and chemoresistance. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5312325 ; http://dx.doi.org/10.5353/th_b5312325 ; http://hdl.handle.net/10722/211053

University of Hong Kong

29. 梅启明; Mei, Qiming. Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock.

Degree: PhD, 2014, University of Hong Kong

URL: Mei, Q. [梅启明]. (2014). Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5204915 ; http://dx.doi.org/10.5353/th_b5204915 ; http://hdl.handle.net/10722/198833

► Circadian rhythmsare biochemical, physiological, and behavioral processes display oscillations of oughly 24-hour, which existing in both prokaryotes and eukaryotes. Circadian rhythms improve fitness of organisms… (more)

▼ Circadian rhythmsare biochemical, physiological, and behavioral processes display oscillations of oughly 24-hour, which existing in both prokaryotes and eukaryotes. Circadian rhythms improve fitness of organisms in both constant and changing environments. The cryptochrome (CRY)and PAS-containing proteins are light sensors and key elements of the circadian system in eukaryotic organisms. Photolyases and cryptochromes are evolutionarily related flavoproteins which perform distinct physiological functions. Photolyases are evolutionarily ancient enzymes that activated by light and repairing UV-induced DNA damage. Although cryptochromes share structural similarity with the DNA photolyases, they lack the DNA repair activity. CRYs are key elements of mammal circadian system, and play roles in light sensing in insects and plants to entrain circadian rhythms. The PAS domains are widely distributed in proteins across all kingdoms of life and act as signal modules. They are common in photoreceptors and transcriptional regulators of eukaryotic circadian clock components including bHLH-PAS proteins (BMAL, CYC,CLK and NPAS2) and PER in animals, PHY and ZTL in plants, WC-1, 2and VVD in fungi. They are mainly involved in protein-protein interaction and light sensing functions. The CRY/PHR superfamily consists of 7 major subfamilies: CPD class I and CPD class II PHRs, (6-4) PHR, CRY-DASH, plant PHR2, plant CRY and animal CRY. Although the superfamily evolved primarily under strong purifying selection (average ω = 0.0178), it experienced strong episodic positive selection at some periods of evolution. The level of variation is subfamily-and domain-specific. The homologs with apparent circadian functions (i.e., plant and animal CRY) are significantly more conserved than the other photolyases. Photolyases were lost in eukaryotic groups like placental mammals, suggesting that natural selection apparently became weaker in the late stage of evolutionary history. The phylogenetic trees of fish Cry features two major clusters, which correspond to Cry1and Cry2. Teleost species possess extra copies of Cry1 due to fish-specific genome duplication (FSGD), and formed 3 clades of Cry1. Clade1B of Cry1(π= 0.129 ±0.062) is more conserved than the other paralogs (πrange from 0.173to 0.195). Test of positive selection revealed that fish cryptochromes evolved under strong purifying selection (average ω= 0.0066).Different fishes preserved different Cry duplicates that associated with reciprocal gene loss, thus generated the diverse circadian molecular mechanisms. The level of DNA variation in the PAS-containing proteins appears to be subfamily-specific. The animal PAS-containing homologs are more polymorphic than the plant and fungal homologs. Although the whole superfamily evolved primarily under strong purifying selection (average ω range from 0.0030to 0.1164), it experienced strong positive selection at some periods of the evolution. Although the PAS domains from different proteins vary in sequence and length, they maintain a fairly… Advisors/Committee Members: Dvornyk, V.

Subjects/Keywords: Circadian rhythms; Transcription factors; Cryptochrome

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APA (6^th Edition):

梅启明; Mei, Q. (2014). Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. (Doctoral Dissertation). University of Hong Kong. Retrieved from Mei, Q. [梅启明]. (2014). Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5204915 ; http://dx.doi.org/10.5353/th_b5204915 ; http://hdl.handle.net/10722/198833

Chicago Manual of Style (16^th Edition):

梅启明; Mei, Qiming. “Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed July 21, 2019. Mei, Q. [梅启明]. (2014). Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5204915 ; http://dx.doi.org/10.5353/th_b5204915 ; http://hdl.handle.net/10722/198833.

MLA Handbook (7^th Edition):

梅启明; Mei, Qiming. “Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock.” 2014. Web. 21 Jul 2019.

Vancouver:

梅启明; Mei Q. Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2019 Jul 21]. Available from: Mei, Q. [梅启明]. (2014). Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5204915 ; http://dx.doi.org/10.5353/th_b5204915 ; http://hdl.handle.net/10722/198833.

Council of Science Editors:

梅启明; Mei Q. Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Mei, Q. [梅启明]. (2014). Molecular evolution of cryptochrome (CRY) and PAS-containing proteins in eukaryotic circadian clock. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5204915 ; http://dx.doi.org/10.5353/th_b5204915 ; http://hdl.handle.net/10722/198833

University of Hong Kong

30. 何兆賢; Ho, Siu-yin, Bryan. Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth.

Degree: PhD, 2014, University of Hong Kong

URL: Ho, S. B. [何兆賢]. (2014). Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5328054 ; http://dx.doi.org/10.5353/th_b5328054 ; http://hdl.handle.net/10722/206748

► The mouse pelage hair consists of three types of hair coined primary (guard), secondary (awls and auchenes) and tertiary (zigzag) hair. They display distinct morphologies… (more)

▼ The mouse pelage hair consists of three types of hair coined primary (guard), secondary (awls and auchenes) and tertiary (zigzag) hair. They display distinct morphologies and are induced consecutively during hair morphogenesis. Previously two identified regulatory mouse mutants, Yellow submarine (Ysb) and Light coat and circling (Lcc) which the chromosomal rearrangements have disrupted the cis-acting regulatory elements of Sox2; resulting in the loss of Sox2 expression in the inner ear. The mutants displayed lighter hair coat color due to a reduction in the proportion of secondary hair and increased proportion of tertiary hair. Sox18 null mutants display darker coat colour and reduced proportion of zigzag hair. To dissect the underlying mechanisms of the phenotypes in hair type specification in 〖Sox2〗^Ysb and 〖Sox2 〗^Lcc mutants and the role of Sox2 and Sox18 in regulating the process; the expression of Sox2 in the hair follicle and the change in the density of hair types in mutants were analyzed. I have identified the expression pattern of Sox2 in the dermal papilla (DP) of the hair follicle and verified its down-regulation in 〖Sox2〗^Ysband 〖Sox2 〗^Lcc mutants. The DP at the base of hair follicle is the signaling center for the regulation of hair development. Sox2 is specifically expressed in the DP of primary and secondary but not in tertiary hair while Sox18 is expressed in the DP of all hair types. Analysis of Sox2 mutants showed that the number of secondary hair was normal at induction but was reduced and accompanied by an increase in tertiary hair in adult mice. The number of tertiary hair was reduced in Sox18 null mutants. To gain insight into the molecular basis of hair type specification and potential targets of Sox2 in the regulation, gene expression profile in DP cells of 〖Sox2 〗^(EGFP/+)and 〖Sox2 〗^(EGFP/Ysb) mice was examined; the data suggests that genes in the Wnt and BMP signalling pathway were down-regulated in Sox2 mutants; while Runx3 and Corin may act downstream of Sox2 in regulating hair type specification and pigmentation. Hair follicles enter cycles of growth and regression throughout life during the hair cycle. Sox2 was only expressed in the growth phase while Sox18 was persistently expressed throughout the hair cycle. I further asked if Sox2 and Sox18 regulate post-natal hair development by analysing the expression pattern of Sox2 and Sox18 in wildtype mice and mutants throughout the hair cycle and the progression of hair growth in the mutants. The growth phase of the first hair cycle was extended in Sox2 mutants while the hair cycle in Sox18 null mutants was normal. Cell proliferation was compromised during hair regeneration leading to a delay in hair regeneration in Sox2 mutants. Sox2 and Sox18 showed overlapping expression in the DP and both regulate hair type specification. To test if Sox2 and Sox18 synergistically regulate hair development, the 〖Sox2〗^(Ysb/Ysb);〖Sox18〗^(-/-) mutants have been generated. Hair morphogenesis and differentiation were impaired; while the number of…

Subjects/Keywords: Hair - Physiology; Transcription factors

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

何兆賢; Ho, Siu-yin, B. (2014). Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. (Doctoral Dissertation). University of Hong Kong. Retrieved from Ho, S. B. [何兆賢]. (2014). Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5328054 ; http://dx.doi.org/10.5353/th_b5328054 ; http://hdl.handle.net/10722/206748

Chicago Manual of Style (16^th Edition):

何兆賢; Ho, Siu-yin, Bryan. “Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed July 21, 2019. Ho, S. B. [何兆賢]. (2014). Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5328054 ; http://dx.doi.org/10.5353/th_b5328054 ; http://hdl.handle.net/10722/206748.

MLA Handbook (7^th Edition):

何兆賢; Ho, Siu-yin, Bryan. “Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth.” 2014. Web. 21 Jul 2019.

Vancouver:

何兆賢; Ho, Siu-yin B. Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2019 Jul 21]. Available from: Ho, S. B. [何兆賢]. (2014). Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5328054 ; http://dx.doi.org/10.5353/th_b5328054 ; http://hdl.handle.net/10722/206748.

Council of Science Editors:

何兆賢; Ho, Siu-yin B. Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Ho, S. B. [何兆賢]. (2014). Genetic analyses of the roles of Sox2 and Sox18 in mouse hair development and growth. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5328054 ; http://dx.doi.org/10.5353/th_b5328054 ; http://hdl.handle.net/10722/206748

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