You searched for subject:(estrogen receptor).
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1.
Magruder, Hilary.
Signaling Effectors Required for G Protein-Coupled Estrogen
Receptor-, GPER, Induced Events Associated with Breast Cancer
Progression.
Degree: PhD, Pathobiology, 2014, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:386260/ 
► Stimulation of estrogen receptor (ER)-negative human breast cancer cells with 17β-estradiol (E2β) results in fibronectin (FN) matrix assembly and transactivation of the epidermal growth factor…
(more)
▼ Stimulation of
estrogen receptor (ER)-negative human
breast cancer cells with 17β-estradiol (E2β) results in fibronectin
(FN) matrix assembly and transactivation of the epidermal growth
factor
receptor (EGFR) via the G protein-coupled
estrogen receptor
(GPER). This mechanism of action results in the recruitment of
FN-engaged integrin α5β1 to fibrillar adhesions and the formation
of integrin α5β1-Shc adaptor protein complexes. Here, we show that
GPER stimulation of murine 4T1 or human SKBR3 breast cancer cells
promotes the formation of focal adhesions, actin stress fibers, and
results in increased cellular adhesion and haptotaxis on FN, but
not collagen. These actions are also induced by the xenoestrogen,
bisphenol A, and the ER antagonist, ICI 182, 780, but not the
inactive stereoisomer, 17α-estradiol (E2α). In addition, we show
that GPER stimulation of breast cancer cells allows for
FN-dependent, anchorage-independent growth and FN fibril formation
in hanging drop assays, indicating that these GPER-mediated actions
occur independently of adhesion to solid substrata. Furthermore,
stable expression of Shc mutant Y317F lacking its primary tyrosyl
phosphorylation site disrupts E2β-induced focal adhesion and actin
stress fiber formation, and abolishes E2β-enhanced haptotaxis on FN
and anchorage-dependent growth. We also show that overexpression of
a phosphatase, PTPN12, known to interact with Shc inhibits focal
adhesion and FN fibril formation, adhesion and haptotaxis on FN,
and anchorage independent growth. Moreover, PTPN12 knockdown
positively influences these events associated with cellular
survival. Collectively, these data demonstrate that E2β action via
GPER enhances cellular adhesivity and FN matrix assembly and allows
for anchorage-independent growth, cellular events that may allow
for cellular survival and tumor progression.
Advisors/Committee Members: Filardo, Edward (Director), Reichner, Jonathan (Reader), Freiman, Richard (Reader), Yang, Wentian (Reader), Prossnitz, Eric (Reader).
Subjects/Keywords: estrogen receptor (ER)
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APA (6th Edition):
Magruder, H. (2014). Signaling Effectors Required for G Protein-Coupled Estrogen
Receptor-, GPER, Induced Events Associated with Breast Cancer
Progression. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:386260/
Chicago Manual of Style (16th Edition):
Magruder, Hilary. “Signaling Effectors Required for G Protein-Coupled Estrogen
Receptor-, GPER, Induced Events Associated with Breast Cancer
Progression.” 2014. Doctoral Dissertation, Brown University. Accessed January 18, 2019.
https://repository.library.brown.edu/studio/item/bdr:386260/.
MLA Handbook (7th Edition):
Magruder, Hilary. “Signaling Effectors Required for G Protein-Coupled Estrogen
Receptor-, GPER, Induced Events Associated with Breast Cancer
Progression.” 2014. Web. 18 Jan 2019.
Vancouver:
Magruder H. Signaling Effectors Required for G Protein-Coupled Estrogen
Receptor-, GPER, Induced Events Associated with Breast Cancer
Progression. [Internet] [Doctoral dissertation]. Brown University; 2014. [cited 2019 Jan 18].
Available from: https://repository.library.brown.edu/studio/item/bdr:386260/.
Council of Science Editors:
Magruder H. Signaling Effectors Required for G Protein-Coupled Estrogen
Receptor-, GPER, Induced Events Associated with Breast Cancer
Progression. [Doctoral Dissertation]. Brown University; 2014. Available from: https://repository.library.brown.edu/studio/item/bdr:386260/
University of Illinois – Urbana-Champaign
2.
Parent, Alexander A.
Second-site inhibitors of the estrogen and androgen hormone receptors.
Degree: PhD, 0335, 2012, University of Illinois – Urbana-Champaign
URL: http://hdl.handle.net/2142/29523
► The estrogen and androgen receptors are members of the nuclear hormone receptor protein superfamily and play an important role in the development of primary and…
(more)
▼ The
estrogen and androgen receptors are members of the nuclear hormone
receptor protein superfamily and play an important role in the development of primary and secondary female and male sexual characteristics. Although necessary for proper development, in certain contexts activation of these receptors contributes to the formation and progression of hyperplastic diseases, namely breast and prostate cancers. Current treatment for metastatic hormone responsive breast and prostate tumors involves either chemical ‘castration’ techniques which target the synthesis of the endogenous
estrogen and androgen agonists, or the administration of hormone antagonists which displace endogenous agonist from the ligand binding domain of the
receptor causing a conformational change such that the transcriptional activity of the protein is inhibited. While efficacious for a duration ranging from a few months to years, breast and prostate tumors eventually cease to respond to these treatments, entering a hormone-refractory state for which there is no adequate treatment.
Multiple new approaches to
estrogen and androgen
receptor inhibition have been reported in recent years. Among these are efforts to directly disrupt the nuclear
receptor/coactivator and the nuclear
receptor/DNA interactions, and to increase degradation of
receptor through binding of small-molecules at non-traditional binding sites. Due to the essential nature of these interactions for
estrogen and androgen
receptor signaling, it has been proposed that such second-site inhibition may be less susceptible to the mutations and
receptor and coregulator overexpression that are currently exhibited in hormone-refractory breast and prostate cancers.
As described herein, we have investigated a number of chemical systems for their ability to disrupt the
estrogen and androgen
receptor/steroid
receptor coactivator interaction. In chapters 2 and 3 we describe the structure-based design of pyrimidine-core small-molecules that mimic the three interacting leucine/phenylalanine residues of the
estrogen and androgen
receptor coactivators. Members of this library bind to both nuclear receptors and disrupt the nuclear
receptor/coactivator complex with Ki’s in the low micromolar range. In our screening against the two subtypes of the
estrogen receptor, we discovered a only few compounds that exhibited binding to the
estrogen receptor beta, and the vast majority show strong preference for
estrogen receptor alpha inhibition. Based on its ability to accommodate larger aromatic residues at the coactivator binding site, we anticipated that pyrimidine-core molecules with bulky aromatic substituents would selectively bind to the androgen
receptor. Indeed, this approach produced multiple coactivator binding inhibitors that displayed potent and selective inhibition of the androgen
receptor, without concomitant disruption of the
estrogen receptor/coactivator complex.
During the synthesis of the pyrimidine-core coactivator binding inhibitors, a tetra-aryl cyclobutane compound that showed potent…
Advisors/Committee Members: Katzenellenbogen, John A. (advisor), Katzenellenbogen, John A. (Committee Chair), van der Donk, Wilfred A. (committee member), Hergenrother, Paul J. (committee member), Gennis, Robert B. (committee member).
Subjects/Keywords: estrogen receptor; androgen receptor; inhibitor; nuclear receptor
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APA (6th Edition):
Parent, A. A. (2012). Second-site inhibitors of the estrogen and androgen hormone receptors. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29523
Chicago Manual of Style (16th Edition):
Parent, Alexander A. “Second-site inhibitors of the estrogen and androgen hormone receptors.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 18, 2019.
http://hdl.handle.net/2142/29523.
MLA Handbook (7th Edition):
Parent, Alexander A. “Second-site inhibitors of the estrogen and androgen hormone receptors.” 2012. Web. 18 Jan 2019.
Vancouver:
Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/2142/29523.
Council of Science Editors:
Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29523
Boston University
3.
Koomson, Jacqueline Nyarkoa.
The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.
Degree: MS, Medical Sciences, 2017, Boston University
URL: http://hdl.handle.net/2144/23835
► Uterine leiomyomas are benign tumors within the uterus, where patients present with symptoms such as abnormal bleeding, urinary retention, and pelvic pressure. The exact etiology…
(more)
▼ Uterine leiomyomas are benign tumors within the uterus, where patients present with symptoms such as abnormal bleeding, urinary retention, and pelvic pressure. The exact etiology of uterine leiomyomas is unknown, but numerous theories have been proposed, indicating a multifactorial mechanism, including lifestyle and steroid hormones. Uterine leiomyomas have become a public health concern due to the high cost of treatment as well as the high prevalence within African American communities. Currently, many treatment options exist, ranging from conservative treatments that address symptoms, to surgical intervention to remove the uterus. Research efforts thus far have determined the relationship between the role of estrogen in the growth of uterine leiomyomas (which has led to development of medications that target different approaches to estrogen synthesis) and its effects in the pathogenesis. Studies have shown that estrogen acts on estrogen receptor subtypes, ER and ER. This study examines the role of these two receptors in estrogenic effects, and how these effects relate to the development of uterine leiomyomas. Available research has shown that each receptor has its unique functions and impacts the growth of tumors differently. There is conflicting evidence in how the number of receptors and surrounding environment modulate leiomyomas, with some studies reporting that it is the corepressors and/or coactivators that ultimately determine the influence of estrogenic effects. However, the general consensus of such studies suggests that estrogen receptor-specific therapeutic intervention is a novel area with great potential. The primary benefit of estrogen receptor-specific treatment, such as selective estrogen receptor modulators, is the ability to regulate physiological processes that contribute to the growth of uterine leiomyomas. Future directions of research include confirming the exact roles of ER and ER and harnessing the effects of their differing functions to manage uterine leiomyomas.
Subjects/Keywords: Medicine; Estrogen; Estrogen receptor alpha; Estrogen receptor beta; Receptor-mediated therapies; Uterine fibroids; Uterine leiomyoma
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APA (6th Edition):
Koomson, J. N. (2017). The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23835
Chicago Manual of Style (16th Edition):
Koomson, Jacqueline Nyarkoa. “The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.” 2017. Masters Thesis, Boston University. Accessed January 18, 2019.
http://hdl.handle.net/2144/23835.
MLA Handbook (7th Edition):
Koomson, Jacqueline Nyarkoa. “The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.” 2017. Web. 18 Jan 2019.
Vancouver:
Koomson JN. The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. [Internet] [Masters thesis]. Boston University; 2017. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/2144/23835.
Council of Science Editors:
Koomson JN. The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23835
Texas A&M University
4.
Lee, Wan-Ru.
Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3).
Degree: 2009, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-1207
► The estrogen receptor (ER) is a ligand-activated transcription factor that regulates gene expression. The classical mechanisms of nuclear ER action include ligand-induced dimerization of ER…
(more)
▼ The
estrogen receptor (ER) is a ligand-activated transcription factor that regulates
gene expression. The classical mechanisms of nuclear ER action include ligand-induced
dimerization of ER which binds
estrogen responsive elements (EREs) in promoters of
target genes. In addition, non-genomic pathways of ER action have also been identified
in breast cancer cells.
Cdc25A is a tyrosine phosphatase that catalyzes dephosphorylation of
cyclin/cyclin-dependent kinase complexes to regulate G1- to S-phase cell cycle
progression. Cdc25A mRNA levels are induced by 17?-estradiol (E2) in ZR-75 breast
cancer cells, and deletion analysis of the Cdc25A promoter identified the -151 to -12
region as the minimal E2-responsive sequence. Subsequent mutation/deletion analysis
showed that at least three different cis-elements were involved in activation of Cdc25A
by E2, namely, GC-rich Sp1 binding sites, CCAAT motifs, and E2F sites. Studies with
inhibitors and dominant negative expression plasmids show that E2 activates Cdc25A
expression through activation of genomic ER?/Sp1 and E2F1 and cAMP-dependent
activation of NF-YA. Thus, both genomic and non-genomic pathways of
estrogen action
are involved in induction of Cdc25A in breast cancer cells.
The PIAS family was initially identified as cytokine-induced inhibitors of STATs
which contain several conserved domains involved in binding to other nuclear
coactivators. In this study we have investigated coactivation of ER? by PIAS3 in breast
cancer cell lines transiently cotransfected with the pERE3 constructs which contain three
tandem EREs linked to a luciferase reporter gene. PIAS3 coactivated ER?-mediated transactivation in cells cotransfected with pERE3 and wild-type ER?. In contrast to many
other coactivators, PIAS3 also enhanced transactivation of ER? when cells were
cotransfected with the TAF1 ER? mutant. In addition, PIAS3 does not interact with
activation function 2 (AF2) domain of ER? in a mammalian two-hybrid assay. These
data indicate that coactivation of ER? by PIAS3 was AF2-domain independent. Analysis
of several PIAS3 deletion mutants showed that the region containing amino acids 274 to
416 of PIAS3 are required for coactivation suggesting that the RING finger domain and
acidic region of PIAS3 are important for interactions with wild-type ER?. These results
demonstrate that PIAS3 coactivated ER? and this represents a non-classical
LXXLL-independent coactivation pathway.
Advisors/Committee Members: Safe, Stephen H. (advisor), Burghardt, Robert C. (committee member), Phillips, Timothy D. (committee member), Porter, Weston W. (committee member).
Subjects/Keywords: Estrogen receptor; Cdc25A; PIAS3
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APA ·
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Manager
APA (6th Edition):
Lee, W. (2009). Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3). (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-1207
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lee, Wan-Ru. “Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3).” 2009. Thesis, Texas A&M University. Accessed January 18, 2019.
http://hdl.handle.net/1969.1/ETD-TAMU-1207.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lee, Wan-Ru. “Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3).” 2009. Web. 18 Jan 2019.
Vancouver:
Lee W. Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3). [Internet] [Thesis]. Texas A&M University; 2009. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1207.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lee W. Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3). [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1207
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Otago
5.
Tran, Khanh Bao.
Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer
.
Degree: 2012, University of Otago
URL: http://hdl.handle.net/10523/2292
► Approximately one in five breast cancer patients exhibits triple negative tumors that are characterized by the lack of estrogen receptor (ER), progesterone receptor and HER2.…
(more)
▼ Approximately one in five breast cancer patients exhibits triple negative tumors that are characterized by the lack of
estrogen receptor (ER), progesterone
receptor and HER2. While ER and HER2 positive tumors are responsive respectively to ER antagonists and anti-HER2 antibodies, triple negative breast cancer (TNBC) tumors do not benefit from any of these therapies. As a result, it is imperative to search for alternative treatments for this subtype. Since synthetic cannbinoids has been shown to possess anticancer effects in a number of other cancer types, we therefore hypothesize that synthetic cannabinoids also have anticancer effects against TNBC tumors. The current study focused on the anticancer potential against TNBC of two synthetic cannabinoids, WIN55,212-2 and JWH-133. In vitro cytotoxicity assessment demonstrated that WIN55,212-2 inhibited the proliferation in vitro of MDA-MB-231 and MDA-MB-468 TNBC cells in a dose-dependent and time-dependent manner; whereas JWH-133 showed no significant cytotoxicity up to 30 µM in MDA-MB-231 and 10 µM in MDA-MB-468 cells. Flow cytometry experiments demonstrated that treatment with WIN55,212-2 (6 µM) for 24 h, 36 h and 48 h significantly increased the proportion of MDA-MB-231 and MDA-MB-468 cells in G1 phase.
In vivo, mice bearing MDA-MB-468 xenografts and treated with WIN55,212-2 (25 µg/day i.p. for 10 weeks) showed a significant 76% reduction in tumour volume compared to vehicle treated mice, and this effect was reversed by 60% by co-treatment with CB2 antagonist AM630. In contrast, JWH-133 (25 µg/day i.p. for 10 weeks) increased tumor volume by 166% compared to vehicle treated mice and this acceleration effect was abolished by co-treatment of AM630. Toxicity profiling studies showed that mice remained healthy after long-term treatment with either WIN55,212-2 or JWH-133 confirmed by no significant change in body weight or major organ weight, and normal plasma ALT levels for each treatment group.
Assessment of
receptor expression status demonstrated the presence of both CB1 and CB2 cannabinoid receptors in MDA-MB-468 xenografts. Importantly, WIN55,212-2 treatment significantly downregulated the expression of both CB1 and CB2 receptors while tended to downregulate EGFR expression. JWH-133 treatment on the other hand was associated with a tendency to activate EGFR. Furthermore, the current study demonstrated for the first time that WIN55,212-2 treatment activated p38 MAPK and inhibited NF-κB expression in the TNBC tumors; whereas JWH-133 treatment tended to activate the survival Akt and β-catenin pathways and the inhibition of p27. The results strongly suggest the diversity in biological effects and complexity in molecular mechanisms of different cannabinnoids, and that a re-consideration on the use of cannabinoids in cancer patients might be needed.
Advisors/Committee Members: Rosengren, Rhonda (advisor).
Subjects/Keywords: cannabinoids;
breast cancer;
estrogen receptor
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APA ·
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APA (6th Edition):
Tran, K. B. (2012). Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer
. (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/2292
Chicago Manual of Style (16th Edition):
Tran, Khanh Bao. “Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer
.” 2012. Masters Thesis, University of Otago. Accessed January 18, 2019.
http://hdl.handle.net/10523/2292.
MLA Handbook (7th Edition):
Tran, Khanh Bao. “Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer
.” 2012. Web. 18 Jan 2019.
Vancouver:
Tran KB. Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer
. [Internet] [Masters thesis]. University of Otago; 2012. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10523/2292.
Council of Science Editors:
Tran KB. Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer
. [Masters Thesis]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2292
Cornell University
6.
Melville, Katherine.
Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading
.
Degree: 2014, Cornell University
URL: http://hdl.handle.net/1813/38857
► Decreased bioavailable estrogen levels are a major cause of bone loss in postmenopausal women, but sex hormones are important regulators of bone mass in both…
(more)
▼ Decreased bioavailable
estrogen levels are a major cause of bone loss in postmenopausal women, but sex hormones are important regulators of bone mass in both sexes.
Estrogen signaling in bone occurs mainly through
estrogen receptors ER[alpha] and ER[beta]. ER[alpha] in particular is important in regulating bone mass and bone's response to mechanical loading, but its particular role in each bone cell type and its cross-talk with BMP signaling are not well studied. ` Osteoblast-specific ER[alpha] knockout (pOC-ER[alpha]KO) and littermate control (LC) were bred by crossing Osteocalcin-Cre and ER[alpha]fl/fl mice. The effects of removing ER[alpha] in osteoblasts and osteocytes on bone mass, bone strength, and bone's response to mechanical loading were studied in 10-week-old animals. In general, cancellous and cortical bone mass were both reduced in pOC-ER[alpha]KO female mice, while bone mass was increased in pOC-ER[alpha]KO male mice compared to their sex-matched LC, measured by microCT in the proximal and midshaft tibia, femur, and L5 vertebra. These bone mass changes correlated with decreased vertebral compressive strength in female knockout mice and increased femoral bending strength in male knockout mice. After two weeks of in vivo tibial compression, female pOC-ER[alpha]KO mice showed a greater increase in bone mass in the proximal tibia, where baseline bone mass was decreased, and at the tibial midshaft, where baseline bone mass was similar to LC. Male pOC-ER[alpha]KO mice exhibited a normal response to mechanical loading. Next, 10-week-old female pOC-ER[alpha]KO and LC mice were administered either RAP-661, a BMPR1a inhibitor, or placebo, and all mice were subjected to daily in vivo tibial compression for two weeks. RAP-661 markedly increased bone mass in the L5 vertebra and cancellous tibial metaphysis of both genotypes, but not at the femoral midshaft, tibial midshaft, or tibial metaphyseal cortex. In the vertebra, the drug-induced increase in bone mass was less in pOC-ER[alpha]KO mice than LC. Animals treated with RAP-661 responded less to mechanical loading in the tibial metaphysis than placebo animals, but similarly at the tibial midshaft. This is the first evidence to indicate that BMPR1a may mediate bone's response to mechanical loading and interact with ER[alpha] in osteoblasts in vivo.
Advisors/Committee Members: Hernandez, Christopher J. (committeeMember), Schimenti, John C. (committeeMember).
Subjects/Keywords: estrogen receptor alpha;
bone;
loading
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APA (6th Edition):
Melville, K. (2014). Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading
. (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/38857
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Melville, Katherine. “Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading
.” 2014. Thesis, Cornell University. Accessed January 18, 2019.
http://hdl.handle.net/1813/38857.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Melville, Katherine. “Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading
.” 2014. Web. 18 Jan 2019.
Vancouver:
Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading
. [Internet] [Thesis]. Cornell University; 2014. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1813/38857.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading
. [Thesis]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/38857
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Manitoba
7.
Chooniedass, Shilpa.
The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.
Degree: Biochemistry and Medical Genetics, 2011, University of Manitoba
URL: http://hdl.handle.net/1993/4421
► In 1999, the discovery of the Steroid Receptor RNA Activator (SRA) was unprecedented in the field of steroid receptor co-regulator research. It was the first…
(more)
▼ In 1999, the discovery of the Steroid
Receptor RNA Activator (SRA) was unprecedented in the field of steroid
receptor co-regulator research. It was the first time that an RNA molecule was demonstrated to function similarly to its protein counterpart and modulate the activity of steroid receptors. This peculiar steroid
receptor co-activator thus attracted the attention of numerous research groups. Over the years, studies were reported deciphering SRA mechanisms of action, its role in co-regulating nuclear receptors and its possible implication in human diseases.
While SRA was originally thought to exist solely as a non-coding RNA, our laboratory has identified longer SRA RNA isoforms with the theoretical capacity to encode for a protein. This discovery impelled us to investigate the existence of a Steroid
Receptor RNA Activator Protein or SRAP. In this thesis, we first demonstrated the existence and function of endogenous evolutionary conserved SRA proteins. Based on these results we further explored SRAP expression in breast tumors. Interestingly, Western blot analysis of a small cohort of
estrogen positive breast tumors suggested that SRAP expression correlates with a better overall survival in patients treated with tamoxifen. This observation prompted us to explore the biological role of SRAP. We found that MCF-7 cells stably expressing coding SRA isoforms had lower ligand dependent
estrogen receptor alpha transcriptional activity. In order to dissect the function of the protein independently of its RNA counterpart, we separated the functions of the protein by introducing extensive silent mutations into the RNA sequence. Using this model, we established that SRAP, independent of its RNA counterpart, enhances
estrogen receptor alpha activity in a ligand and response-element dependent manner. Furthermore, we showed for the first time that SRAP physically interacts with multiple transcription factors and is recruited to specific promoter regions. Moreover, by artificially recruiting SRAP to the promoter of a luciferase reporter gene under the control of the strong transcriptional activator VP16, we observed a decrease in transcription. These latter results suggest that SRA could function as a repressor through direct association with promoters.
Overall, we believe that SRA is a very peculiar example of a bi-faceted system consisting of a functional RNA and its corresponding protein. Altogether our data suggest that SRAP, similarly to its RNA counterpart, is involved in many critical pathways that directly participate in gene expression regulation.
Advisors/Committee Members: Leygue, Etienne (Biochemistry and Medical Genetics) (supervisor), Murphy, Leigh (Biochemistry and Medical Genetics) Davie, Jim (Biochemistry and Medical Genetics) Xie, Juiyong (Physiology) (examiningcommittee).
Subjects/Keywords: steoid receptor RNA activator; estrogen receptor
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APA (6th Edition):
Chooniedass, S. (2011). The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4421
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chooniedass, Shilpa. “The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.” 2011. Thesis, University of Manitoba. Accessed January 18, 2019.
http://hdl.handle.net/1993/4421.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chooniedass, Shilpa. “The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.” 2011. Web. 18 Jan 2019.
Vancouver:
Chooniedass S. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. [Internet] [Thesis]. University of Manitoba; 2011. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1993/4421.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chooniedass S. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. [Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4421
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Houston
8.
Butler, Ryan 1986-.
Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.
Degree: Biology and Biochemistry, Department of, 2013, University of Houston
URL: http://hdl.handle.net/10657/956
► Ligand-activated transcription factors are a diverse group of proteins that are involved a variety of physiological processes. The purpose of these studies was to investigate…
(more)
▼ Ligand-activated transcription factors are a diverse group of proteins that are involved a variety of physiological processes. The purpose of these studies was to investigate the aryl hydrocarbon
receptor (AhR) knockout mouse and the effects of hormone replacement therapy on the postmenopausal breast in order to better understand the functions of the ligand-activated transcription factors AhR and
estrogen receptor β (ERβ).
In the first part of these studies, we investigated the AhR knockout mouse in order to further elucidate the physiological functions of AhR. These mice developed stones in their urinary bladders composed of 100% uric acid while the serum uric acid levels remained normal. We determined these stones were formed by the breakdown of DNA into uric acid from a large number of dying cells. These mice also develop fibrosis of their ventral prostates and a phenotype in the immune system similar to chronic myeloid leukemia.
The second part of these studies was to investigate the effects of hormone replacement therapy on the histology and expression of various ligand-activated transcription factors in the postmenopausal breast. We treated postmenopausal women with
estrogen or
estrogen-progesterone therapy for 3 months and took biopsies of the breasts before and after treatment. Expression of several proteins including AhR, ERα, and ERβ were unchanged after treatment while expression of progesterone receptors was increased. Proliferation and breast density were unchanged by treatment in these breasts;
however, we show possible mechanisms leading to proliferation and development of density in non-cancerous breast tissue.
In conclusion, these studies revealed a role for AhR in prostatic development, uric acid formation, and leukemia, and have provided new information on the safety of short-term use of HRT.
Advisors/Committee Members: Gustafsson, Jan-Åke (advisor), Warner, Margaret (committee member), Ziburkus, Jokubas (committee member), Webb, Paul (committee member).
Subjects/Keywords: aryl hydrocarbon receptor; estrogen receptor; transcription factor
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APA (6th Edition):
Butler, R. 1. (2013). Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. (Thesis). University of Houston. Retrieved from http://hdl.handle.net/10657/956
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Butler, Ryan 1986-. “Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.” 2013. Thesis, University of Houston. Accessed January 18, 2019.
http://hdl.handle.net/10657/956.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Butler, Ryan 1986-. “Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.” 2013. Web. 18 Jan 2019.
Vancouver:
Butler R1. Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. [Internet] [Thesis]. University of Houston; 2013. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10657/956.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Butler R1. Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. [Thesis]. University of Houston; 2013. Available from: http://hdl.handle.net/10657/956
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
9.
Tan, Susanna Shu Xian.
Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling.
Degree: 2016, University of Toronto
URL: http://hdl.handle.net/1807/76045
► Estrogens exert their effects by activating estrogen receptor alpha (ERα) and beta (ERβ). A number of different co-regulator proteins regulate the activities of both receptors.…
(more)
▼ Estrogens exert their effects by activating estrogen receptor alpha (ERα) and beta (ERβ). A number of different co-regulator proteins regulate the activities of both receptors. Identifying new ER co-regulators could lead to improved treatments for diseases, such as breast cancer. This study aimed to characterize the role of TIPARP, a mono-ADP-ribosyltransferase and novel co-regulator of ERs. Gene expression and ChIP studies revealed that TIPARP mRNA levels were regulated by ERs, and that ERα was recruited to TIPARP. TIPARP in turn repressed ERα, but co-activated ERβ activity. Furthermore, TIPARP was recruited to the regulatory regions of estrogen target genes. TIPARP mono-ADP-ribosylated both ERα and ERβ and reversed the effects of the mono-ADP-ribosylase, MacroD1, on ERα/β transactivation. Taken together, this work showed that TIPARP is a mixed function co-regulator of ERs, revealing that TIPARP and MacroD1 dynamically regulate the activities of ERα/β through ADP-ribosylation.
M.Sc.
Advisors/Committee Members: Matthews, Jason, Pharmacology.
Subjects/Keywords: Estrogen; Estrogen Receptor; Nuclear transcription factors; Receptor Signalling; TIPARP; 0307
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APA (6th Edition):
Tan, S. S. X. (2016). Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/76045
Chicago Manual of Style (16th Edition):
Tan, Susanna Shu Xian. “Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling.” 2016. Masters Thesis, University of Toronto. Accessed January 18, 2019.
http://hdl.handle.net/1807/76045.
MLA Handbook (7th Edition):
Tan, Susanna Shu Xian. “Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling.” 2016. Web. 18 Jan 2019.
Vancouver:
Tan SSX. Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1807/76045.
Council of Science Editors:
Tan SSX. Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/76045
University of Rochester
10.
Hsu, Iawen.
The Roles of Estrogen Receptors in the Bladder Cancer
Development.
Degree: PhD, 2013, University of Rochester
URL: http://hdl.handle.net/1802/27302
► Early studies documented the existence of sexual dimorphism in bladder cancer occurrence and progression with higher bladder cancer incidence in males than females. However, the…
(more)
▼ Early studies documented the existence of sexual
dimorphism in bladder cancer occurrence and progression with higher
bladder cancer incidence in males than females. However, the
progression of bladder cancer after diagnosis is more rapid in
females than males. These contrasting differences could be due to
the differential effects of female hormones-estrogens, and their
binding receptors including ERα and ERβ on the bladder cancer
incidence and progression. Results from recent studies using
various in vitro cell lines and in vivo mouse models demonstrate
differential roles of ERs in cancer initiation and progression such
that ERα suppresses bladder cancer initiation and invasion whereas
ERβ promotes bladder cancer initiation and progression. Mechanistic
studies indicate ERα and ERβ may act through modulation of the AKT
activity/pathway or DNA replication complex, respectively, to
influence bladder cancer progression. Targeting ER signaling
pathways using various selective ER subtype modulators may lead to
the development of new therapeutic approaches to control bladder
cancer progression.
Subjects/Keywords: Estrogen Receptor Alpha; Estrogen Receptor Beta; MCM5; Bladder Cancer BBN; Inpp4β
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APA ·
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MLA ·
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CSE |
Export
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APA (6th Edition):
Hsu, I. (2013). The Roles of Estrogen Receptors in the Bladder Cancer
Development. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27302
Chicago Manual of Style (16th Edition):
Hsu, Iawen. “The Roles of Estrogen Receptors in the Bladder Cancer
Development.” 2013. Doctoral Dissertation, University of Rochester. Accessed January 18, 2019.
http://hdl.handle.net/1802/27302.
MLA Handbook (7th Edition):
Hsu, Iawen. “The Roles of Estrogen Receptors in the Bladder Cancer
Development.” 2013. Web. 18 Jan 2019.
Vancouver:
Hsu I. The Roles of Estrogen Receptors in the Bladder Cancer
Development. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1802/27302.
Council of Science Editors:
Hsu I. The Roles of Estrogen Receptors in the Bladder Cancer
Development. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27302
Univerzitet u Beogradu
11.
Božović, Ana M., 1977-.
Metilovanje promotora i ekspresija estrogenskog receptora
beta (ERß) u invazivnim karcinomima dojke.
Degree: Biološki fakultet, 2014, Univerzitet u Beogradu
URL: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get
► Biologija - Molekularna genetika kancera / Biology - Molecular genetics of cancer
Invazivni karcinom dojke je najčešći kancer kod žena. Pored genetičkih i epigenetički faktori…
(more)
▼ Biologija - Molekularna genetika kancera / Biology
- Molecular genetics of cancer
Invazivni karcinom dojke je najčešći kancer kod
žena. Pored genetičkih i epigenetički faktori imaju važnu ulogu u
njegovoj inicijaciji i progresiji. Cilj ove studije bio je ispitati
da li metilacija promotora ON, gena za ERβ protein (ESR2) utiče na
njegovu ekspresiju (na nivou iRNK i proteina) i utvrditi povezanost
metilacionog indeksa promotora ON sa nivoima ERβ1-iRNK i ERβ1
proteina, kao i sa kliničkim i patohistološkim parametrima. U ovoj
studiji analiziran je 131 arhivski uzorak kancera dojke. Pomoću
posebno dizajniranog PCR testa iz dva koraka, amplifikovan je i
kvantifikovan specifični region promotora ON ESR2 gena. Za
kvantifikaciju ERβ1-iRNK korišćena je metoda kvantitativnog RT-PCR
u realnom vremenu. Metoda „Western Blot“ je korišćena za relativnu
kvantifikaciju ERβ1 proteinske izoforme. Dobijeni podaci,
metilacioni indeks promotora ON, nivoi iRNK i ERβ1 proteina,
analizirani su i korelisani sa kliničkopatološkim parametrima
neparametrijskim statističkim testovima. Nađeno je da je
metilacioni indeks promotora ON ERβ gena značajno veći u grupi
pacijentkinja sa pozitivnim, u odnosu na grupu sa negativnim
statusom aksilarnih limfnih čvorova. Takođe, pronađena je značajna
pozitivna korelacija metilacionog indeksa promotora ON ERβ gena sa
nivoom estrogenskog receptora α. Na osnovu dobijenih rezultata
pokazano je da metilacioni indeks promotora ON, ERβ gena može biti
pouzdaniji marker prognoze kancera dojke nego ekspresija ERβ1-iRNK
ili proteina ERβ1.
Advisors/Committee Members: Mandušić, Vesna.
Subjects/Keywords: Breast cancer; estrogen receptor alpha; estrogen
receptor beta; progesterone receptor; methylation; quantitative
PCR
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APA ·
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APA (6th Edition):
Božović, Ana M., 1. (2014). Metilovanje promotora i ekspresija estrogenskog receptora
beta (ERß) u invazivnim karcinomima dojke. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Božović, Ana M., 1977-. “Metilovanje promotora i ekspresija estrogenskog receptora
beta (ERß) u invazivnim karcinomima dojke.” 2014. Thesis, Univerzitet u Beogradu. Accessed January 18, 2019.
https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Božović, Ana M., 1977-. “Metilovanje promotora i ekspresija estrogenskog receptora
beta (ERß) u invazivnim karcinomima dojke.” 2014. Web. 18 Jan 2019.
Vancouver:
Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora
beta (ERß) u invazivnim karcinomima dojke. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2019 Jan 18].
Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora
beta (ERß) u invazivnim karcinomima dojke. [Thesis]. Univerzitet u Beogradu; 2014. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Guelph
12.
Ervin, Kelsy.
The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice
.
Degree: 2014, University of Guelph
URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818
► Social learning is a process by which an animal gains information from another; however much of the research on estrogens effects on learning focuses on…
(more)
▼ Social learning is a process by which an animal gains information from another; however much of the research on estrogens effects on learning focuses on individual learning tasks. We therefore examined the effects of 17-estradiol (17beta-E2) and agonists for the
estrogen receptors (ERs) ER-alpha, ER-beta, and the G protein-coupled ER 1 (GPER1) on the social transmission of food preferences (STFP) task, within a time scale allowing us to determine the rapid effects of estrogens. General ER activation with 17beta-E2 rapidly improved social learning on this task. Specific activation of the GPER1 also rapidly improved social learning, suggesting that 17beta-E2 acts through the GPER1 to rapidly improve learning on the STFP. Activation of ER-alpha and ER-beta activation, however, induced some impairing effects on learning. Rapid estrogenic modulation of social learning in the STFP therefore likely depends on the receptors activated, as each ER differently affected learning on this task.
Advisors/Committee Members: Choleris, Elena (advisor).
Subjects/Keywords: estradiol; social transmission of food preference; estrogen receptor alpha; estrogen receptor beta; G protein-coupled estrogen receptor; GPER; GPR30
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APA (6th Edition):
Ervin, K. (2014). The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice
. (Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ervin, Kelsy. “The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice
.” 2014. Thesis, University of Guelph. Accessed January 18, 2019.
https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ervin, Kelsy. “The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice
.” 2014. Web. 18 Jan 2019.
Vancouver:
Ervin K. The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice
. [Internet] [Thesis]. University of Guelph; 2014. [cited 2019 Jan 18].
Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ervin K. The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice
. [Thesis]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Cornell University
13.
Hah, Nasun.
Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses
.
Degree: 2011, Cornell University
URL: http://hdl.handle.net/1813/33589
► Estrogens play crucial roles in regulating gene expression in physiological and disease states. Estrogens acts through estrogen receptors (ERs) and their binding sites in genomic…
(more)
▼ Estrogens play crucial roles in regulating gene expression in physiological and disease states. Estrogens acts through
estrogen receptors (ERs) and their binding sites in genomic DNA to modulate transcription by RNA polymerase II. Although recent gene-specific and genomic analyses have provided considerable information about of
estrogen-dependent transcription, many aspects of the
estrogen signaling network have not yet been elucidated. The goal of my studies was to uncover new information about the immediate and direct effects of
estrogen signaling at the cell membrane, in the cytoplasm, and in the nucleus to elucidate the underlying regulatory networks. First, I investigated an ER transcriptional coregulators, SWI/SNF, an ATPdependent chromatin remodeling complex. I explored the molecular functions of the BAF57 and BAF180 subunits of SWI/SNF using a quantitative proteomic approach called SILAC (Stable Isotope Labeling by Amino Acids in Cell Culture). I found that depletion of BAF57 results in a significant depletion of BAF180 from the SWI/SNF complex without decreasing the total cellular BAF180 levels, resulting in an accumulation of cells in the G2/M phase. Knockdown of BAF57 also causes transcriptional misregulation of cell cycle-related genes involved in the late G2 checkpoint. Collectively, these studies have elucidated the role of BAF57 and BAF180 in the transcriptional control of cell proliferation. Second, I have used GRO-Seq (Global Nuclear Run-On and Massively Parallel Sequencing) to explore the immediate effects of
estrogen signaling on the transcriptome of breast cancer cells. I found that
estrogen directly regulates a strikingly large fraction of the transcriptome in a rapid, robust, and unexpectedly transient manner. In addition to protein coding genes,
estrogen regulates the distribution and activity of all three RNA polymerases, and virtually every class of non-coding RNA that has been described to date. I also identified a large number of previously undetected
estrogen-regulated intergenic transcripts, many of which are found proximal to ER[alpha] binding sites. These results provide the most comprehensive measurement of the primary and immediate
estrogen effects to date. I expect that genome-wide inferences based on the direct
estrogen-regulated transcriptome in combination with
estrogen-regulated signaling pathway will be useful for understanding
estrogen biology.
Advisors/Committee Members: Collins, Ruth N. (committeeMember), Lis, John T (committeeMember).
Subjects/Keywords: estrogen;
estrogen receptor;
GRO-seq;
swi/snf;
baf57;
baf180;
silac;
proteomic;
enhancer;
edc;
estrogen signaling
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Manager
APA (6th Edition):
Hah, N. (2011). Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses
. (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/33589
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses
.” 2011. Thesis, Cornell University. Accessed January 18, 2019.
http://hdl.handle.net/1813/33589.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses
.” 2011. Web. 18 Jan 2019.
Vancouver:
Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses
. [Internet] [Thesis]. Cornell University; 2011. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1813/33589.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses
. [Thesis]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/33589
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Texas A&M University
14.
Wu, Fei.
Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors.
Degree: 2009, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2433
► Estrogen receptor ? (ER?) is a ligand activated transcription factor. Many widely used synthetic compounds and natural chemicals can activate ER?. The compounds investigated in…
(more)
▼ Estrogen receptor ? (ER?) is a ligand activated transcription factor. Many widely
used synthetic compounds and natural chemicals can activate ER?. The
compounds investigated in this study include 17?-estradiol (E2), diethylstilbestrol
(DES), antiestrogens ICI 182,780, 4-hydroxytamoxifen, the phytoestrogen
resveratrol, and the xenoestrogens bisphenol A (BPA), nonylphenol (NP),
octylphenol (OP), endosulfan, kepone, 2,2-bis(p-hydroxyphenyl)-1,1,1-
trichloroethane (HPTE) and 2,3,4,5-tetrachlorobiphenylol-4-ol (HO-PCB-Cl4).
With the exception of the antiestrogens, all the compounds induced
transactivation in MCF-7 or MDA-MB-231 cells transfected with wild-type ER?
and a construct (pERE3) containing three tandem
estrogen responsive elements
(EREs) linked to a luciferase gene. However, these compounds differentially
activated C-terminal deletion mutants of ER?. For example, neither E2 nor DES
induced transactivation in MCF-7 transfected with ER?(1-537) due to partial
deletion of helix 12 of ER?; however, OP, NP, resveratrol, kepone and HPTE
induced this ER? mutant, demonstrating that the estrogenic activity of these
synthetic compounds do not require activation function 2 (AF-2) of ER?.
This study also investigated the effects of xenoestrogens on activation of
reporter gene activity in MCF-7 and MDA-MB-231 cells transfected with a
construct (pSp13) containing three tandem GC-rich Sp binding sites linked to the
luciferase gene. In MCF-7 cells, antiestrogen-induced activation of ER?/Sp1 required the zinc finger motifs of ER?, whereas activation by
estrogen and some
xenoestrogens activation, such as endosulfan, NP and OP required the H12 of
ER?. In contrast, xenoestrogens, such as HPTE, BPA, kepone and HO-PCBCl4,
significantly induced transactivation of all four ER? deletion mutants tested
in this study. Moreover, RNA interference assays demonstrated structuredependent
differences in activation of ER?/Sp1, ER?/Sp3 and ER?/Sp4.
The in vivo activities of E2, ICI 182,780, BPA and NP were further investigated
in a transgenic mouse model containing pSp13 transgene. All the compounds
induced luciferase activity in the mouse uterus; however activities observed in
the penis and testis of male and stomach of both male and female mice were
structure-dependent,.
These results demonstrate that various ER ligands differentially activate ER? in
breast cancer cells and transgenic mice, and their activities are dependent on
ER? variants, promoter-, cell-context and selective use of different Sp proteins,
suggesting these structurally diverse compounds are selective ER modulators
(SERMs).
Advisors/Committee Members: Safe, Stephen (advisor), Burghardt, Robert (committee member), Kunkel, Gary (committee member), Sacchettini, James (committee member).
Subjects/Keywords: estrogen receptor; endocrine disruptors; breast cancer
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wu, F. (2009). Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2433
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Wu, Fei. “Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors.” 2009. Thesis, Texas A&M University. Accessed January 18, 2019.
http://hdl.handle.net/1969.1/ETD-TAMU-2433.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Fei. “Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors.” 2009. Web. 18 Jan 2019.
Vancouver:
Wu F. Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors. [Internet] [Thesis]. Texas A&M University; 2009. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2433.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu F. Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors. [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2433
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Texas A&M University
15.
Armstrong, Cameron Michelle.
The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.
Degree: 2013, Texas A&M University
URL: http://hdl.handle.net/1969.1/151883
► Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein…
(more)
▼ Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein aim to determine the protective mechanisms of estradiol (E2) during sporadic and inflammation-associated colonic carcinogenesis.
When investigating the role of E2 and fish oil at the earliest stage of sporadic colon cancer development, E2 had no effect on DNA adduct formation while dietary fish oil significantly reduced DNA adduct formation. Contrarily, E2 significantly induced apoptosis of damaged colonocytes while fish oil was not protective.
In an in vivo model of inflammation-associated colon carcinogenesis with E2 administered following induction of DNA damage and initiation of inflammation, E2 treatment was associated with decreased colon tumor size and number in wild type (WT) but not
estrogen receptor (ER) ? knockout (ER?KO) mice. Interestingly, apoptosis was reduced and proliferation increased by E2 in these tumors in WT mice. This may be due to the altered ER expression in these tissues as the tumors developed, with ER??expression decreasing concomitantly with ER? expression increasing.
Contrary to the protective effect of E2 on inflammation-associated colon tumor formation, which was dependent on ER?, during acute inflammation in the colon E2 was protective against inflammation in both WT and ER?KO mice and injury in ER?KO mice. The protection against inflammation is likely due to the reduction of pro-inflammatory cytokine expression by E2. Apoptosis and proliferation were decreased and increased in the proximal and distal colon respectively in ER?KO mice.
In vitro studies further elucidated the roles of ER? and ER? in colonocytes. E2 and ER?, but not ER?, specific agonists reduced cell number and induce apoptosis in nonmalignant colonocytes. This effect was lost in the presence of mutated p53. In ER? overexpressed nonmalignant colonocytes, E2 had no effect on cell number while ER? agonist and ER? agonists decreased and increased cell number respectively.
These studies suggest that E2 is protective in the colon and ER? is required for protection against carcinogenesis but not protection against inflammation. Additionally, the protection against colon carcinogenesis is likely p53 mediated.
Advisors/Committee Members: Allred, Clinton D (advisor), Turner, Nancy D (committee member), Villalobos, Alice R (committee member), Weeks, Brad R (committee member).
Subjects/Keywords: colon cancer; estradiol; estrogen receptor; inflammation
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APA (6th Edition):
Armstrong, C. M. (2013). The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151883
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Thesis, Texas A&M University. Accessed January 18, 2019.
http://hdl.handle.net/1969.1/151883.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Web. 18 Jan 2019.
Vancouver:
Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Internet] [Thesis]. Texas A&M University; 2013. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1969.1/151883.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151883
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Georgia State University
16.
Russell, Nancy.
Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen.
Degree: MS, Biology, 2010, Georgia State University
URL: https://scholarworks.gsu.edu/biology_theses/25
► Male rat sexual behavior requires aromatization of testosterone (T) to estradiol (E2) in the medial preoptic area (MPO) where estrogen receptors (ER) exist in…
(more)
▼ Male rat sexual behavior requires aromatization of testosterone (T) to estradiol (E2) in the medial preoptic area (MPO) where
estrogen receptors (ER) exist in two isoforms, ERα and ERβ. We hypothesized that E2 acts through
estrogen receptor α (ERα) in the MPO to promote male mating behavior. Four groups of male rats were castrated, administered DHT s.c. and bilateral MPO implants delivering either: cholesterol, E2, propyl pyrazole triol (PPT, ERα agonist), diarylpropionitrile (DPN, ER β agonist), or 1-methyl-4-phenyl pyridinium (MPP, ERα antagonist). Additional gonadally intact males received bilateral MPO DPN implants. PPT maintained sexual behavior equally as well as E2, whereas mating was not maintained by cholesterol or DPN MPO implants. Exogenous T did not reinstate mating in animals that received MPP MPO implants. These findings indicate that, in the MPO, ERα is necessary and sufficient to promote copulatory behavior in male rats and ERβ is not sufficient for mating.
Advisors/Committee Members: Dr. Andrew Clancy, Dr. Matthew Grober, Dr. Kyle Frantz.
Subjects/Keywords: Medial preoptic area; Estrogen receptor; Estradiol
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APA (6th Edition):
Russell, N. (2010). Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/biology_theses/25
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Russell, Nancy. “Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen.” 2010. Thesis, Georgia State University. Accessed January 18, 2019.
https://scholarworks.gsu.edu/biology_theses/25.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Russell, Nancy. “Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen.” 2010. Web. 18 Jan 2019.
Vancouver:
Russell N. Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen. [Internet] [Thesis]. Georgia State University; 2010. [cited 2019 Jan 18].
Available from: https://scholarworks.gsu.edu/biology_theses/25.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Russell N. Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen. [Thesis]. Georgia State University; 2010. Available from: https://scholarworks.gsu.edu/biology_theses/25
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Canterbury
17.
Graham, Lisa Anne.
Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.
Degree: Chemistry, 2012, University of Canterbury
URL: http://hdl.handle.net/10092/7173
► Environmental xenoestrogens (EEs) are chemicals that when they enter the body, the body responds to them as it would to endogenous estrogens. Humans are exposed…
(more)
▼ Environmental xenoestrogens (EEs) are chemicals that when they enter the body, the body
responds to them as it would to endogenous estrogens. Humans are exposed to these
chemicals on a daily basis via natural components, additives and contaminants in food and
water, through the use of pharmaceuticals and personal care products such as sunscreens,
lotions and toothpaste. Exposure to EEs is thought to result in adverse effects on humans
such as decreased fertility, increased susceptibility to hormone-sensitive cancers, deformities
of the male genitalia and precocious puberty in females. The critical window of exposure is
thought to be early fetal development, when tissues are rapidly differentiating under the
control of endogenous estrogens. However, there is limited data in the literature on human
fetal exposure to EEs. The first objective of this study was to assess human fetal exposure to
a suite of 35 EEs by analysis of paired samples of amniotic fluid and maternal urine were
collected from 32 New Zealand women between 14 and 20 weeks gestation. The analytical
chemistry methods required for this study were developed and validated. The results
demonstrate that fetal exposure is highly correlated with maternal exposure. This study is the
first to report maternal urine levels of two UV filters and amniotic fluid levels of parabens,
UV filters and triclosan. A model based on simple additivity of effect was developed that
combined the measured concentrations with literature data on relative estrogenic potency to
assess the magnitude of the estrogen signal that may be attributed to the EEs. This model
suggests that the fetus may experience an estrogen signal due to the measured EEs that could
be as large as the endogenous estrogen signal. A second objective was to use computational
docking to study the interactions of the EEs with the human estrogen receptor (hER) protein.
The docking studies show that the rigid endogenous ligand, 17β-estradiol (E2) interacts with
the hER to produce a single, well-defined complex with the receptor and the flexible EEs
produce multiple, distinct energy-equivalent complexes. EEs are not able to interact with the
binding cavity to stabilise the rigid hER-E2-like topology of the complex. As a result, the
hER-EE complexes can be thought of as more pliable or ‘floppy’ and thus able to respond to
the cell context in multiple ways, leading to variations in gene expression in different target
tissues. These multiple pathways may explain the range of physiological responses attributed
to exposure that depend on the timing of exposure and the sex of the individual exposed.
Subjects/Keywords: Estradiol; human effects; gestational exposure; estrogen receptor
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APA (6th Edition):
Graham, L. A. (2012). Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. (Thesis). University of Canterbury. Retrieved from http://hdl.handle.net/10092/7173
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Graham, Lisa Anne. “Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.” 2012. Thesis, University of Canterbury. Accessed January 18, 2019.
http://hdl.handle.net/10092/7173.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Graham, Lisa Anne. “Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.” 2012. Web. 18 Jan 2019.
Vancouver:
Graham LA. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. [Internet] [Thesis]. University of Canterbury; 2012. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10092/7173.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Graham LA. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. [Thesis]. University of Canterbury; 2012. Available from: http://hdl.handle.net/10092/7173
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Virginia Tech
18.
Rajalekshmi Devi, Sarika.
Development of Novel anti-estrogens for endocrine resistant Breast Cancer.
Degree: MS, Chemistry, 2016, Virginia Tech
URL: http://hdl.handle.net/10919/81275
► ER+ breast cancer raises a significant diagnostic challenge since resistance invariably develops to the current endocrine therapies. 70% of breast cancers are ER+, which results…
(more)
▼ ER+ breast cancer raises a significant diagnostic challenge since resistance invariably develops to the current endocrine therapies. 70% of breast cancers are ER+, which results from the overexpression of
estrogen receptor. ER mediates strong anti-inflammatory signaling in ER+ tissues. Once activated with estradiol (E2), ER inhibits inflammatory gene expression via protein-protein interactions that block NF-kappa B transcriptional activity. Importantly, NF-kappa B is a primary mediator of resistance in many cancers, including breast cancer. All current endocrine suppressive treatments block this palliative signaling pathway, along with the desired proliferative pathway. Thus, there is a significant unmet clinical need for novel endocrine treatments for breast cancer that can ameliorate patient outcome in resistant populations, be less prone to resistance development, retain anti-inflammatory action, and cause fewer side effects.
Following the hypothesis driven approach, the work described here introduces structural analogs of an innovative ligand scaffold, 5,6-bis-(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hept-5-ene-2-sulfonic acid phenyl ester, termed OBHS, which reduces gene activation through ligand-induced shifts in helices 8 and 11, thereby indirectly modulating helix 12 of ER (hence, indirect antagonists). This new class of ligands with a bicyclic hydrophobic core retains strong anti-inflammatory effects while dialing out the proliferative effects of E2 (similar to Selective
Estrogen Receptor Modulators, SERMS), and could potentially replace the current endocrine therapies of breast cancer. In this work, we carried out rational design and syntheses of two series of OBHS analogs, namely OBHS-A (for acetamido derivatives), and OBHS-P (for propargyl derivatives), while we explored a synthetic methodology for a third series of OBHS compounds.
Many analogs from the OBHS-A series exhibited high binding affinity. For example, the exo diastereomer of 2.11a, 2.11b, 2.11c, 2.11d, and 2.11e exhibited Relative Binding Affinities (RBAs) of 22.6%, 10.5%, 19.5%, 12.1%, and 14.4%, respectively. As observed before, endo OBHS compounds exhibited lower binding affinities than exo compounds. The RBA values with acetamide, and isobutyramide (i.e. short hydrophobic chains) were very comparable to each other. However, unexpectedly the propionamide compound showed lower binding affinity than butyramide. Nevertheless, we consider OBHS analogs with RBA values greater than 1% (Kd = 20 nM) to be very potent. This data is only the first step in a battery of assays that will be conducted eventually on these compounds. In particular, our emphasis is in ascertaining and improving the NF-kappa B mediated anti-inflammatory property, where these compounds have shown promising activity in conjunction with their anti-proliferative activity.
Advisors/Committee Members: Josan, Jatinder (committeechair), Kingston, David G (committee member), Santos, Webster (committee member).
Subjects/Keywords: Chemistry; organic; breast cancer; estrogen receptor; OBHS
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APA (6th Edition):
Rajalekshmi Devi, S. (2016). Development of Novel anti-estrogens for endocrine resistant Breast Cancer. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/81275
Chicago Manual of Style (16th Edition):
Rajalekshmi Devi, Sarika. “Development of Novel anti-estrogens for endocrine resistant Breast Cancer.” 2016. Masters Thesis, Virginia Tech. Accessed January 18, 2019.
http://hdl.handle.net/10919/81275.
MLA Handbook (7th Edition):
Rajalekshmi Devi, Sarika. “Development of Novel anti-estrogens for endocrine resistant Breast Cancer.” 2016. Web. 18 Jan 2019.
Vancouver:
Rajalekshmi Devi S. Development of Novel anti-estrogens for endocrine resistant Breast Cancer. [Internet] [Masters thesis]. Virginia Tech; 2016. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10919/81275.
Council of Science Editors:
Rajalekshmi Devi S. Development of Novel anti-estrogens for endocrine resistant Breast Cancer. [Masters Thesis]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/81275
Vanderbilt University
19.
Pruitt, Freddie Lee.
A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis.
Degree: PhD, Cancer Biology, 2013, Vanderbilt University
URL: http://etd.library.vanderbilt.edu/available/etd-06242013-125056/
;
► Stromal-epithelial interactions are important in both prostate development and cancer. Stromal changes have been shown to be powerful prognostic indicators of prostate cancer progression and…
(more)
▼ Stromal-epithelial interactions are important in both prostate development and cancer. Stromal changes have been shown to be powerful prognostic indicators of prostate cancer progression and of patient death helping to define lethal versus indolent phenotypes. The specific molecular underpinnings of these interactions are incompletely understood. Several molecules found to be aberrantly expressed in cancer associated fibroblasts (CAFs) (including cyclin D1 [CD1], stromal derived factor 1 [SDF-1]) contribute to tumorigenesis and malignant transformation in xenograft experiments. These molecules can be regulated by a number of different factors, but are both putative
estrogen regulated genes. In this study, we show that dysregulation of ERα expression in cancer associated stroma results in the differential regulation of
estrogen responsive genes that are key factors in enhancing the invasive potential of the epithelial tumor. The cell cycle regulator CD1 and the
estrogen receptor are known to interact and can induce estrogenic gene transcription. Cathepsin D (CathD) is an
estrogen regulated aspartic endopeptidase, known to be involved in a number of physiological processes as well as in the regulation of apoptosis. In this study, we highlight CathD as a mediator of cancer associated stromal promotion of prostate tumorigenesis. An examination of human prostate tissue revealed significantly increased stromal staining of CathD in malignant prostate tissue in comparison to benign prostate tissue. Stromal specific overexpression of CathD in benign prostate stromal cells induced malignancy in adjacent epithelium through increased TGFβ signaling and responsive gene expression. The proteolytic function of stromally-derived CathD is dependent on the activity of hydrogen-proton pump activity on the surface of prostate epithelial cell lines. The study presented here indicates that CathD is not only an important mediator of stroma-epithelial cross talk, but also an essential component in promotion of tumorigenesis in vivo, and Inhibition of ER signaling in the cancer associated stroma inhibits malignant transformation in the adjacent epithelium.
Advisors/Committee Members: Simon W. Hayward (committee member), Robert Matusik (chair), Barbara Fingleton (committee member), Fritz Parl (committee member).
Subjects/Keywords: Stroma; microenvironment; estrogen receptor; cathepsin D
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APA (6th Edition):
Pruitt, F. L. (2013). A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;
Chicago Manual of Style (16th Edition):
Pruitt, Freddie Lee. “A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed January 18, 2019.
http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;.
MLA Handbook (7th Edition):
Pruitt, Freddie Lee. “A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis.” 2013. Web. 18 Jan 2019.
Vancouver:
Pruitt FL. A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2019 Jan 18].
Available from: http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;.
Council of Science Editors:
Pruitt FL. A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;
20.
Van der Plas, Steven.
Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors.
Degree: 2009, Ghent University
URL: http://hdl.handle.net/1854/LU-505579
► Worldwide concern has been growing on the increasing distribution of endocrine disrupting chemicals (EDCs) during the last decade. The overall anxiety is caused by their…
(more)
▼ Worldwide concern has been growing on the increasing distribution of endocrine disrupting chemicals (EDCs) during the last decade. The overall anxiety is caused by their effect on the endocrine system of wildlife and humans. While the influence on the reproductive systems of several animals has been thoroughly documented, the effects on human health are still the
subject of intense debate. Establishing a causal relationship between the presence of EDCs in the environment and their possible effects on human health is a challenging quest. Besides their low physiologically active concentrations, the complex environmental matrices in which they are present, makes it very difficult to identify and quantify different EDCs. This problem can be tackled by a pre-concentration step before the actual analysis. In general, solid-phase extraction (SPE) of aqueous samples is a widly applied technique to enrich pollutants. With the current SPE cartridges, the extraction efficiency of the pollutants depends on their polarity. Thus polar compounds stay in the water sample while apolar compounds are retained on the solid phase. As a consequence the selectivity of the SPE is poor. A solid-phase material which could selectively bind the different EDCs would thus greatly simplify the analysis. This PhD will focus on the development of an artificial
receptor that shows high affinity towards common EDCs and low or no affinity to other compounds present in environmental samples. By constructing this
receptor on a solid phase, a new affinity based SPE material can be developed, resulting in a more accurate and selective determination of EDCs.
Advisors/Committee Members: Madder, Annemieke.
Subjects/Keywords: Chemistry; EDC; solid phase; estrogen receptor
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APA (6th Edition):
Van der Plas, S. (2009). Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors. (Thesis). Ghent University. Retrieved from http://hdl.handle.net/1854/LU-505579
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Van der Plas, Steven. “Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors.” 2009. Thesis, Ghent University. Accessed January 18, 2019.
http://hdl.handle.net/1854/LU-505579.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Van der Plas, Steven. “Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors.” 2009. Web. 18 Jan 2019.
Vancouver:
Van der Plas S. Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors. [Internet] [Thesis]. Ghent University; 2009. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1854/LU-505579.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Van der Plas S. Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors. [Thesis]. Ghent University; 2009. Available from: http://hdl.handle.net/1854/LU-505579
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Ottawa
21.
Boucher, Julie.
Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring
.
Degree: 2015, University of Ottawa
URL: http://hdl.handle.net/10393/32957
► Cigarette smoking during pregnancy contributes to the development of neurological health problems in offspring. As a result, public health organizations are recommending NRT to pregnant…
(more)
▼ Cigarette smoking during pregnancy contributes to the development of neurological health problems in offspring. As a result, public health organizations are recommending NRT to pregnant women to wean them off tobacco. If nicotine itself is injurious to the developing brain, then nicotine substitution may not eliminate the deleterious health outcomes of maternal smoking. In studies of cognitive decline, estradiol elicits a neuroprotective effect through ER activation. However, the underlying mechanism remains unclear. Evidence suggests that estrogen-mediated neuroprotection is activated through glial cell interaction, mitigating inflammation and protecting neurons critical for learning and memory. If NRT antagonizes these cellular targets, it may put individuals at risk for future cognitive impairments. Randomly assigned nulliparous female Wistar rats were injected subcutaneously with 1 mg/kg/day of nicotine bitartrate or saline for 2 weeks before mating until weaning (PND 21). Pups (saline n=6 and nicotine, n=6) were sacrificed at 26 weeks of age and the hippocampal formation was processed for Nissl and immunohistochemical staining for GFAP and ERα. Gestational exposure to nicotine only produced a significant increase in the expression of ERα in the DG of the hippocampus. While additional research is needed, these findings suggest that NRT might indeed interfere with proper brain development, making offspring increasingly susceptible to long-term adverse health effects.
Le tabac fumé pendant la grossesse affecte de manière importante le développement neurologique de la progéniture, y compris à long terme. C’est pourquoi, les autorités de la santé publique recommandent les substituts nicotiniques comme soutien au sevrage tabagique chez les femmes enceintes. Si le danger se situe dans la nicotine de la cigarette, alors les produits de substitution nicotiniques risquent également d’interférer avec le développement cérébral. De nombreuses données expérimentales convergent pour attribuer un rôle protecteur à l’oestradiol sur le fonctionnement cognitif. Par contre, le mécanisme sous-jacent est inconnu. Il se peut que l’oestradiol arrive à neutraliser la réaction inflammatoire provoquée par les cellules gliales, amoindrissant la détérioration des neurones impliqués au niveau de la mémoire. Ainsi, une perturbation de ce mécanisme par la nicotine pourrait engendrer une détérioration progressive des fonctions cognitives. Des rats femelles Wistars nullipares assignées de façon alléatoire à un groupe ont reçu soit une injection sous-cutanée de 1mg/kg/jour de nicotine bitartrate ou de saline, 2 semaines avant l’accouplement jusqu'au sevrage au jour 21 postnatal. A 26 semaines, les ratons furent sacrifiés (saline n=6 et nicotine, n=6) et une analyse du Nissl et immunohistochimique de GFAP et ERα furent réalisées sur les formations hippocampiques. L’exposition prénatale à la nicotine a…
Subjects/Keywords: nicotine;
estrogen receptor;
immunohistochemistry;
astrocyte;
neuron
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Export
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APA (6th Edition):
Boucher, J. (2015). Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/32957
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Boucher, Julie. “Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring
.” 2015. Thesis, University of Ottawa. Accessed January 18, 2019.
http://hdl.handle.net/10393/32957.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Boucher, Julie. “Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring
.” 2015. Web. 18 Jan 2019.
Vancouver:
Boucher J. Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring
. [Internet] [Thesis]. University of Ottawa; 2015. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10393/32957.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Boucher J. Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring
. [Thesis]. University of Ottawa; 2015. Available from: http://hdl.handle.net/10393/32957
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Houston
22.
-8465-3791.
Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.
Degree: Biology and Biochemistry, Department of, 2015, University of Houston
URL: http://hdl.handle.net/10657/2018
► Despite its slow development and our capacity for early detection using endoscopy, colorectal cancer remains the second leading cause of cancer death in the United…
(more)
▼ Despite its slow development and our capacity for early detection using endoscopy, colorectal cancer remains the second leading cause of cancer death in the United States. Epidemiological studies indicate a role for
estrogen in protecting against colorectal cancer.
Estrogen receptor β (ERβ) has been found to be the main ER in the colon. Cell line studies have implicated that ERβ has anti-tumorigenic and anti-proliferative effects on colon cancer cells lines while human epidemiological data suggest that polymorphisms in the ERβ gene are associated with greater cancer risk and lower survival.
Overexpression of ERβ changes the miRnome. Here we show that ERβ can alleviate the progression of colon cancer by inhibiting proliferation through decreasing MYC transcription and therefore decreasing levels of miR-17-92 (OncomiR-1). This is reflected in a decrease in cell number, decrease in migration, and increase in apoptosis. Furthermore, addition of miR-17 using miRNA mimics reverses the effects of ERβ. This demonstrates that ERβ influences not only the transcriptome, but also the miRnome and that the miRnome can be potential targets for novel treatment approaches.
ERβ upregulates miR-205 and downregulates PROX1. This study uncovers the pathway in which ERβ downregulates the transcription factor PROX1 by upregulating miR-205 directly. MiR-205 then targets PROX1 mRNA for degradation. This results in the cells adopting a more adhesive phenotype and reduces the metastatic potential. This study uncovers the potential for ERβ to be anti-metastatic in addition to being anti-proliferative and anti-inflammatory.
ERβ modulates the NFkB inflammatory cascade. One of ERβ’s attributes is that it has anti-inflammatory capabilities. Using a whole genome approach, this study reveals that ERβ can modulate the NFkB inflammatory network. In SW480 cells, ERβ downregulates NFkB transcription factors and induces apoptosis. In HT29 cells, ERβ prevents p65 subunit of NFkB from translocating to the nucleus. Overall, ERβ attenuates the NFkB signaling cascade by attenuating genes related to inflammation while enhancing genes related to apoptosis and cellular defenses. This makes ERβ a useful target for anti-inflammatory drug treatments for patients suffering from chronic inflammatory diseases.
Advisors/Committee Members: Williams, Cecilia M. (advisor), Lin, Chin-Yo (committee member), Gunaratne, Preethi H. (committee member), Lee, Mong-Hong (committee member).
Subjects/Keywords: Estrogen receptor beta; colon cancer epithelial cells
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APA (6th Edition):
-8465-3791. (2015). Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. (Thesis). University of Houston. Retrieved from http://hdl.handle.net/10657/2018
Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
-8465-3791. “Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.” 2015. Thesis, University of Houston. Accessed January 18, 2019.
http://hdl.handle.net/10657/2018.
Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
-8465-3791. “Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.” 2015. Web. 18 Jan 2019.
Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Vancouver:
-8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. [Internet] [Thesis]. University of Houston; 2015. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10657/2018.
Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
-8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. [Thesis]. University of Houston; 2015. Available from: http://hdl.handle.net/10657/2018
Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation
Duquesne University
23.
Kirker, Mary Rachel.
The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development.
Degree: PhD, Pharmacology-Toxicology, 2009, Duquesne University
URL: https://dsc.duq.edu/etd/750
► The increased risk of age-related cataracts in postmenopausal women and studies in animal models suggest that estrogen may have a protective role in the lens.…
(more)
▼ The increased risk of age-related cataracts in postmenopausal women and studies in animal models suggest that
estrogen may have a protective role in the lens. However, very little is known regarding the role of
estrogen and its receptors in the lens. To begin unraveling the
estrogen signaling mechanism in the lens, the following aims were investigated: 1) to determine if
estrogen receptors are expressed in the lens, [125I]-17beta-estradiol binding and mRNA expression of ERalpha, ERbeta, and GPR30 were examined in the mouse and human lens; 2) to determine if the loss of ERalpha and/or ERbeta receptors will induce spontaneous development of cataracts and to examine their role in an inducible cataract model; and 3) to identify
estrogen-regulated genes in the lens that influence cataract development in the ERdelta3-induced cataract model. High-affinity, saturable binding sites for 17beta-estradiol were identified in the nuclear, cytosolic, and membrane fractions of the mouse and human lens. Additionally, detectable binding in the membrane fraction and expression of GPR30 mRNA in the mouse and human lens are the first evidence of this novel transmembrane
estrogen receptor in the lens of any species. Transcripts for ERalpha, ERbeta, and GPR30 were expressed in the mouse lens which suggests that one or more of these
estrogen receptor subtypes are responsible for the binding detected. With the loss of nuclear ER in the lens, spontaneous cataracts did not occur; however, diminished levels or loss of ERalpha in ERdelta3 female mice increased the severity of cortical cataracts with age. These results suggest that ERalpha in the lens may provide protection against the progression of cataracts in the ERdelta3 model. Together with the cataract induction and gene expression studies, six genes were identified to be differentially expressed with
estrogen versus vehicle treatment in the lenses of ERdelta3 mice. The pax6, tcfap2a, tgfbeta2, six3, sox2, and pdgfalpha genes are known to have a critical role in lens development, proliferation, differentiation and maintenance of lens homeostasis. Therefore, future examination of these genes and their pathways in the lens may contribute to the understanding of the mechanisms of
estrogen-mediated protection of lens transparency. Knowledge of pathways that function to maintain lens transparency and how
estrogen regulated these pathways will assist in the development of
estrogen therapies that can be clinically used to delay the onset and/or progression of cataracts.
Advisors/Committee Members: Vicki Davis, Jane Cavanaugh, Carmen Colitz, Kyle Selcer, Paula Witt-Enderby.
Subjects/Keywords: Cataract; Estrogen Receptor; Human; Lens; Mouse
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APA (6th Edition):
Kirker, M. R. (2009). The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development. (Doctoral Dissertation). Duquesne University. Retrieved from https://dsc.duq.edu/etd/750
Chicago Manual of Style (16th Edition):
Kirker, Mary Rachel. “The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development.” 2009. Doctoral Dissertation, Duquesne University. Accessed January 18, 2019.
https://dsc.duq.edu/etd/750.
MLA Handbook (7th Edition):
Kirker, Mary Rachel. “The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development.” 2009. Web. 18 Jan 2019.
Vancouver:
Kirker MR. The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development. [Internet] [Doctoral dissertation]. Duquesne University; 2009. [cited 2019 Jan 18].
Available from: https://dsc.duq.edu/etd/750.
Council of Science Editors:
Kirker MR. The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development. [Doctoral Dissertation]. Duquesne University; 2009. Available from: https://dsc.duq.edu/etd/750
Texas A&M University
24.
Weige, Charles.
Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.
Degree: 2012, Texas A&M University
URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838
► Hormone replacement therapy and estrogen replacement therapy have shown the ability to reduce risk of colon cancer development in clinical and animal studies, but in…
(more)
▼ Hormone replacement therapy and
estrogen replacement therapy have shown the ability to reduce risk of colon cancer development in clinical and animal studies, but in vitro research has been unable to reproduce an estradiol (E2) induced response in colon cancer cell lines. We demonstrated that young adult mouse colonocytes (YAMC, non-malignant colonocytes) exhibit an anti-proliferative response to E2 treatment. These cells demonstrate reduced cell culture growth and increased apoptosis in response to E2. YAMC cells containing an activated Ras mutation are considered to be malignantly transformed, and lose the ability to respond to E2 treatment. Fulvestrant (ICI) was used as an
estrogen receptor antagonist to determine that these results were
estrogen receptor mediated. Furthermore, this effect was demonstrated to require the presence of ER? through the use of a transgenic ERbeta knockout mouse. In these mice, the presence of E2 significantly reduced the formation of azoxymethane induced premalignant lesions.
Since YAMC cells exhibit an anti-proliferative response to E2 treatment, we utilized isogenic YAMC cell lines with and without a dominant negative p53 mutation to demonstrate that this E2 induced action involves p53 activity. E2 treatment results in increased p53 transcriptional activity and a pro-apoptotic change in expression of p53 downstream targets. Presence of the dominant negative p53 mutant nullifies these effects of E2 treatment.
The involvement of p53 in the previously described protection against AOM induced premalignant lesions, was investigated using wild type and heterozygous p53 knockout (Het p53KO) mice. The reduction in p53 protein corresponded to reduced effectiveness of E2 treatment on the prevention of premalignant lesion formation in Het p53KO mice.
In summary, our data indicate that E2 treatment induces anti-proliferative responses in non-malignant colonocytes and protects against the formation of carcinogen-induced premalignant lesions. These effects require the presence of functional ER? and p53. Further studies are required to more thoroughly elucidate the specific interactions and downstream effects of ER? and p53 in response to E2 stimulation.
Advisors/Committee Members: Allred, Clinton D. (advisor), Chapkin, Robert S. (committee member), Dabney, Alan R. (committee member), Lupton, Joanne R. (committee member).
Subjects/Keywords: Estrogen; estrogen receptor beta; colon cancer; p53; apoptosis; aberrant crypt foci
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APA (6th Edition):
Weige, C. (2012). Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Weige, Charles. “Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.” 2012. Thesis, Texas A&M University. Accessed January 18, 2019.
http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Weige, Charles. “Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.” 2012. Web. 18 Jan 2019.
Vancouver:
Weige C. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. [Internet] [Thesis]. Texas A&M University; 2012. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Weige C. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. [Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Kansas
25.
Wang, Pan.
Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp.
Degree: PhD, Pharmacology, Toxicology & Therapeutics, 2010, University of Kansas
URL: http://hdl.handle.net/1808/7432
► The endogenous estrogens are vitally-important female sex hormones with diverse biological functions. Disruption of their actions contributes to the pathogenesis of a number of disease…
(more)
▼ The endogenous estrogens are vitally-important female sex hormones with diverse biological functions. Disruption of their actions contributes to the pathogenesis of a number of disease states in humans, such as endocrine disruption, infertility, and development of cancers. My dissertation research sought to explore the potential usefulness of computational molecular modeling tools in studying the interactions of various
estrogen derivatives (e.g., endogenous
estrogen metabolites, non-aromatic steroids, and synthetic antiestrogens) with human ERs as well as a recently-identified intracellular
estrogen-binding protein. The results of my dissertation projects offer important insights into the three-dimensional structural characteristics of the binding interactions of various
estrogen analogs with the human ERs and PDIp. These studies provide a platform for the future development of an automated docking-based computational approach that can screen numerous environmental compounds for their potential ability to bind to human ERs as well as other
estrogen binding proteins in the body.
Advisors/Committee Members: Zhu, Bao Ting (advisor), Hagenbuch, Bruno (cmtemember), Klaassen, Curtis D. (cmtemember), Petroff, Brian K. (cmtemember), Weir, Scott J (cmtemember).
Subjects/Keywords: Pharmacology; Antiestrogen; Estrogen; Estrogen receptor; Molecular docking; Molecular modeling; Pdip
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APA (6th Edition):
Wang, P. (2010). Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/7432
Chicago Manual of Style (16th Edition):
Wang, Pan. “Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp.” 2010. Doctoral Dissertation, University of Kansas. Accessed January 18, 2019.
http://hdl.handle.net/1808/7432.
MLA Handbook (7th Edition):
Wang, Pan. “Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp.” 2010. Web. 18 Jan 2019.
Vancouver:
Wang P. Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp. [Internet] [Doctoral dissertation]. University of Kansas; 2010. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/1808/7432.
Council of Science Editors:
Wang P. Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp. [Doctoral Dissertation]. University of Kansas; 2010. Available from: http://hdl.handle.net/1808/7432
University of Cincinnati
26.
Minges, Cheryl.
Targeted Deletion of Estrogen Receptor Alpha in Mouse
Pituitary Lactotrophs.
Degree: MS, Pharmacy: Pharmaceutical Sciences, 2011, University of Cincinnati
URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494
► Prolactin (PRL) is a major anterior pituitary (AP) hormone that is necessary for mammary gland development, lactation, and female fertility. The synthesis and release…
(more)
▼ Prolactin (PRL) is a major anterior pituitary
(AP) hormone that is necessary for mammary gland development,
lactation, and female fertility. The synthesis and release of PRL
from specialized pituitary cells (lactotrophs) is tightly regulated
and primarily under tonic inhibition by dopamine (DA), produced by
the tuberoinfundibular dopaminergic neurons (TIDA) of the
hypothalamus. In turn, PRL regulates its own release by acting on
the TIDA neurons in a short feedback loop to increase inhibition by
DA and maintain homeostasis. Superimposed on this negative
regulation are the stimulatory effects of
estrogen.
Estrogen (E2)
stimulates PRL synthesis, secretion, and lactotroph proliferation
by direct action at the level of the AP. E2 also stimulates PRL
indirectly at the level of the hypothalamus by inhibiting TIDA
activity. Finally, E2 can also modify lactotroph response to DA and
other PRL-regulatory factors. The normal growth and function of
lactotrophs depends on an interactive balance between DA and E2.
However, the relative contribution of E2 regulation directly on the
pituitary lactotrophs versus hypothalamic DA, particularly during
various physiological states in the female, is not well defined and
current animal models are unable to distinguish this. Thus, there
is a need for a new model with which to study the regulatory role
of E2 action at the level of the pituitary versus the hypothalamus.
Through transgenic Cre/loxP technology and homologous
recombination, we have generated a selective knockout mouse model
in which the primary mediator of E2 action in the lactotroph,
estrogen receptor alpha (ERa), is deleted only in pituitary
lactotrophs, while conserving E2 action at the TIDA neurons. Herein
is the generation of this animal model and its characterization.
Results show the successful generation of mice with the ERa
knockout targeted to lactotrophs but not in other ERa expressing
tissues of these animals.
Estrogen responsiveness
of the selective knockout mouse was evaluated. In vivo studies,
utilizing a model of spontaneous prolactinoma formation, showed no
significant differences in AP growth between mice with the
selective deletion of ERa and those without. DA levels in the AP
were low in both groups, suggesting that loss of dopaminergic
inhibition contributes more to lactotroph proliferation than does a
direct action of E2 however further investigation is required to
support this conclusion. In vitro studies demonstrated that
lactotrophs with ERa deletion did not respond to E2 or E2
antagonist with regard to cell content of PRL, highlighting the
direct action of E2 on the lactotroph in modulating PRL synthesis.
Our mouse model, with selective loss of ERa in pituitary
lactotrophs, and E2 action at the level of the hypothalamus
maintained, will provide an effective tool in elucidating the
primary effects of
estrogen, as well as other factors, on PRL
regulation.
Advisors/Committee Members: Gregerson, Karen (Committee Chair).
Subjects/Keywords: Pharmaceuticals; Lactotrophs; Anterior Pituitary; Estrogen; Prolactin; Dopamine; Estrogen Receptor
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APA (6th Edition):
Minges, C. (2011). Targeted Deletion of Estrogen Receptor Alpha in Mouse
Pituitary Lactotrophs. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494
Chicago Manual of Style (16th Edition):
Minges, Cheryl. “Targeted Deletion of Estrogen Receptor Alpha in Mouse
Pituitary Lactotrophs.” 2011. Masters Thesis, University of Cincinnati. Accessed January 18, 2019.
http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494.
MLA Handbook (7th Edition):
Minges, Cheryl. “Targeted Deletion of Estrogen Receptor Alpha in Mouse
Pituitary Lactotrophs.” 2011. Web. 18 Jan 2019.
Vancouver:
Minges C. Targeted Deletion of Estrogen Receptor Alpha in Mouse
Pituitary Lactotrophs. [Internet] [Masters thesis]. University of Cincinnati; 2011. [cited 2019 Jan 18].
Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494.
Council of Science Editors:
Minges C. Targeted Deletion of Estrogen Receptor Alpha in Mouse
Pituitary Lactotrophs. [Masters Thesis]. University of Cincinnati; 2011. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494
University of Western Australia
27.
Dennis, Maxine Elizabeth.
Oestrogen and atherosclerosis.
Degree: PhD, 2008, University of Western Australia
URL: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01
► [Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a…
(more)
▼ [Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative effect of hormone replacement therapy (HRT) on cardiovascular disease (CVD) risk amongst postmenopausal women. It is important to determine how a hormone with numerous positive effects on intermediate pathways of atherosclerosis fails to offer cardioprotection. Further investigation into the actions of oestrogen in the vasculature may add to our current understanding of the pathogenesis of atherosclerosis and oestrogen biology. The primary aim of this thesis was to investigate involvement of the oestrogen receptors (ERs) in atherosclerotic CVD and to provide further insight into the actions of oestrogen on the vasculature by studying the actions of oestrogen on the regulation of an oestrogen-responsive gene within human vascular cells. Following confirmation of ERα and ERβ expression at the RNA and protein level in human aorta sections, correlations of receptor expression with age and atherosclerosis were examined. Significantly strong negative relationships of ERα, androgen receptor (AR), and progesterone receptor (PR) with age in both males and females were detected. No trend was detected between ERβ expression and age. These findings suggest that the receptor-mediated actions of hormones in the vasculature may change with age. Further, this thesis compared for the first time sex hormone receptor expression in normal and adjacent atherosclerotic aortic tissue providing a critical assessment of receptor differences due to atherosclerosis. Results revealed reductions of all hormone receptors in early atherosclerotic versus normal aorta tissue. ... These results suggest that the 3'-UTR SNPS may have more of an influence on carotid thickening when oestrogen levels are lower, suggesting the importance of both genetic variation of the ERβ gene and oestrogen status on carotid thickening. Finally, this was the first study to investigate oestrogen-induced regulation of angiotensinogen (AGT), a candidate gene for CVD, in human vascular cells. Oestrogen influenced AGT transcription in a cell specific manner. The overall influence of oestrogen on AGT transcription in the vasculature is unknown. This thesis adds to the knowledge of oestrogen and atherosclerosis by suggesting the involvement of the sex hormone receptors (ERα, ERβ, PR and AR) in atherosclerosis, presenting ERβ as a potentially important candidate gene for atherosclerosis, revealing interactions between estrogen status and associations of ERβ SNPs with carotid thickening, and demonstrating vascular cell-specific actions of oestrogen on the regulation of a candidate gene for CVD. These factors may have contributed to the lack of cardio-protection following HRT, as revealed by large clinical trials.
[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative…
Subjects/Keywords: Angiotensins; Atherosclerosis; Estrogen; Estrogen; Atherosclerosis; Oestrogen receptor; Angiotensinogen
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APA (6th Edition):
Dennis, M. E. (2008). Oestrogen and atherosclerosis. (Doctoral Dissertation). University of Western Australia. Retrieved from http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01
Chicago Manual of Style (16th Edition):
Dennis, Maxine Elizabeth. “Oestrogen and atherosclerosis.” 2008. Doctoral Dissertation, University of Western Australia. Accessed January 18, 2019.
http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01.
MLA Handbook (7th Edition):
Dennis, Maxine Elizabeth. “Oestrogen and atherosclerosis.” 2008. Web. 18 Jan 2019.
Vancouver:
Dennis ME. Oestrogen and atherosclerosis. [Internet] [Doctoral dissertation]. University of Western Australia; 2008. [cited 2019 Jan 18].
Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01.
Council of Science Editors:
Dennis ME. Oestrogen and atherosclerosis. [Doctoral Dissertation]. University of Western Australia; 2008. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01
University of Manchester
28.
Smith, Matthew John.
Exploring the effects of estrogen receptor beta polymorphisms on wound repair.
Degree: PhD, 2017, University of Manchester
URL: https://www.research.manchester.ac.uk/portal/en/theses/exploring-the-effects-of-estrogen-receptor-beta-polymorphisms-on-wound-repair(af2ae557-16ef-43a2-b5a7-db541b7c5d65).html
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703017
► Estrogen is an important regulator and promoter of epithelial wound healing. This is facilitated by increased keratinocyte and fibroblast migration and proliferation, as well as…
(more)
▼ Estrogen is an important regulator and promoter of epithelial wound healing. This is facilitated by increased keratinocyte and fibroblast migration and proliferation, as well as promotion of angiogenesis, matrix deposition and inflammatory response dampening. The potential to target this pathway for therapeutics is highlighted by observations that post-menopausal women on hormone replacement therapy have a significantly lower incidence of venous ulcers. Previous work from this laboratory identified four SNPs (single nucleotide polymorphisms) in the 5’UTR of estrogen receptor beta (ERβ) gene that are associated with venous ulcer predisposition. Disease association is further supported by the identification of ERβ as the main conduit of the beneficial effects of estrogen signalling on wound healing. SNP’s of the 5’UTR can affect transcriptional expression through the modification of transcription factor binding sites, epigenetic modifications and translational efficiency via mRNA localisation and secondary structure alterations. To investigate the possible biological function of these SNPs, we have developed disease relevant cell based assays where primary keratinocyte and fibroblast cells were selected harbouring disease-associated SNPs. We demonstrate that the presence of venous ulcer-associated ERβ SNPs reduced the expression of ERβ in skin cells and reduced their migration and proliferative capabilities. Evidence gathered here suggests that ERβ expression is curtailed by a change in transcription factor binding, likely facilitated by the change in nucleotide sequence brought about by the rs2987983 SNP. Further, we demonstrate that SNP-induced changes in fibroblast expression of growth factors and inflammatory mediators can hinder keratinocyte migration and induce a pro-inflammatory phenotype in human monocytes. Lastly, RNAseq analysis of keratinocytes reveals a SNP-dependant gene expression profile that is detrimental to wound healing. This work provides the first evidence of a direct functional link between venous ulcer-associated ERβ SNPs and dysfunctional wound healing. Investigating ERβ SNPs has provided insight into novel mechanisms of estrogen signalling that can be applied for therapeutic development to treat venous ulcers.
Subjects/Keywords: 617.1; Estrogen; Wound healing; Wound; Estrogen receptor; ERß; ESR2
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APA (6th Edition):
Smith, M. J. (2017). Exploring the effects of estrogen receptor beta polymorphisms on wound repair. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/exploring-the-effects-of-estrogen-receptor-beta-polymorphisms-on-wound-repair(af2ae557-16ef-43a2-b5a7-db541b7c5d65).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703017
Chicago Manual of Style (16th Edition):
Smith, Matthew John. “Exploring the effects of estrogen receptor beta polymorphisms on wound repair.” 2017. Doctoral Dissertation, University of Manchester. Accessed January 18, 2019.
https://www.research.manchester.ac.uk/portal/en/theses/exploring-the-effects-of-estrogen-receptor-beta-polymorphisms-on-wound-repair(af2ae557-16ef-43a2-b5a7-db541b7c5d65).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703017.
MLA Handbook (7th Edition):
Smith, Matthew John. “Exploring the effects of estrogen receptor beta polymorphisms on wound repair.” 2017. Web. 18 Jan 2019.
Vancouver:
Smith MJ. Exploring the effects of estrogen receptor beta polymorphisms on wound repair. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2019 Jan 18].
Available from: https://www.research.manchester.ac.uk/portal/en/theses/exploring-the-effects-of-estrogen-receptor-beta-polymorphisms-on-wound-repair(af2ae557-16ef-43a2-b5a7-db541b7c5d65).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703017.
Council of Science Editors:
Smith MJ. Exploring the effects of estrogen receptor beta polymorphisms on wound repair. [Doctoral Dissertation]. University of Manchester; 2017. Available from: https://www.research.manchester.ac.uk/portal/en/theses/exploring-the-effects-of-estrogen-receptor-beta-polymorphisms-on-wound-repair(af2ae557-16ef-43a2-b5a7-db541b7c5d65).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703017
University of North Carolina – Wilmington
29.
Perry, Heather N.
Synthesis of compounds capable of producing cytotoxic
N3-methyladenine DNA adducts in estrogen receptor positive
cells.
Degree: 2009, University of North Carolina – Wilmington
URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760
► This project describes the design and synthesis of new compounds that are capable of targeting cells that express the estrogen receptor and producing cytotoxic N3-methyladenine…
(more)
▼ This project describes the design and synthesis of new
compounds that are capable of targeting cells that express the
estrogen receptor and producing cytotoxic N3-methyladenine DNA
adducts in those cells. These compounds contain a reactive
methylsulfonate group connected to a unit that binds to DNA in the
minor groove at adenine-thymine rich regions, and therefore,
selectively methylates adenines in these regions at the N3
position. This component is connected by a linking unit to
estradiol, which binds to the
estrogen receptor, and therefore, is
expected to selectively target these compounds to cells that
express the
estrogen receptor. The linking unit is the only
variable component in the design, and can be altered in order to
optimize the DNA and
estrogen receptor binding properties of the
compound, and to modulate the water solubility of the compounds.
The synthesis of three compounds varying in linker length by one,
two, and three methylene units is described.; Cell receptors, DNA
adducts – Synthesis, Estrogen – Receptors, Selective
estrogen
receptor modulators
Advisors/Committee Members: Sridhar Varadarajan (advisor).
Subjects/Keywords: Cell receptors; DNA adducts – Synthesis; Estrogen – Receptors; Selective estrogen receptor modulators
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APA (6th Edition):
Perry, H. N. (2009). Synthesis of compounds capable of producing cytotoxic
N3-methyladenine DNA adducts in estrogen receptor positive
cells. (Masters Thesis). University of North Carolina – Wilmington. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760
Chicago Manual of Style (16th Edition):
Perry, Heather N. “Synthesis of compounds capable of producing cytotoxic
N3-methyladenine DNA adducts in estrogen receptor positive
cells.” 2009. Masters Thesis, University of North Carolina – Wilmington. Accessed January 18, 2019.
http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760.
MLA Handbook (7th Edition):
Perry, Heather N. “Synthesis of compounds capable of producing cytotoxic
N3-methyladenine DNA adducts in estrogen receptor positive
cells.” 2009. Web. 18 Jan 2019.
Vancouver:
Perry HN. Synthesis of compounds capable of producing cytotoxic
N3-methyladenine DNA adducts in estrogen receptor positive
cells. [Internet] [Masters thesis]. University of North Carolina – Wilmington; 2009. [cited 2019 Jan 18].
Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760.
Council of Science Editors:
Perry HN. Synthesis of compounds capable of producing cytotoxic
N3-methyladenine DNA adducts in estrogen receptor positive
cells. [Masters Thesis]. University of North Carolina – Wilmington; 2009. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760
30.
Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Yuya.
Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy.
Degree: 博士(医学), 2017, University of Miyazaki / 宮崎大学
URL: http://hdl.handle.net/10458/5983
► 学位論文の一部を構成しているため、http://hdl.handle.net/10458/5984 に本文を掲載。
Although estrogen is implicated in the regulation of cell growth and differentiation in many organs, the exact mechanism for liver regeneration is not…
(more)
▼ 学位論文の一部を構成しているため、http://hdl.handle.net/10458/5984 に本文を掲載。
Although estrogen is implicated in the regulation of cell growth and differentiation in many organs, the exact mechanism for liver regeneration is not completely understood. We investigated the effect of estrogen on liver regeneration in male and female Wistar rats after 70% partial hepatectomy (PHx) and performed immunohistochemistry, western blotting and Southwestern histochemistry. 17β-estradiol (E2) and ICI 182,780 were injected into male rats on the day before PHx. The proliferating cell nuclear antigen (PCNA) labeling index reached a maximum at 48 hr after PHx in males, and at 36 hr in females and E2-treated male rats. Estrogen receptor α (ERα) was expressed in zones 1 and 2 in male rats, but was found in all zones in female rats. Interestingly, ERα was not detected at 6–12 hr after PHx but was found at 24–168 hr in male rats. However, ERα expression was found at all sampling time-points in female and E2-treated male rats. The activity of estrogen responsive element binding proteins was detected from 12 hr after PHx in male rats but was found from 6 hr in female and E2-treated male rats. ERα was co-expressed with PCNA during liver regeneration. These results indicate that estrogen may play an important role in liver regeneration through ERα.
Subjects/Keywords: estrogen; estrogen receptor α; liver regeneration; partial hepatectomy; cell proliferation
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Y. (2017). Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy. (Thesis). University of Miyazaki / 宮崎大学. Retrieved from http://hdl.handle.net/10458/5983
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Yuya. “Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy.” 2017. Thesis, University of Miyazaki / 宮崎大学. Accessed January 18, 2019.
http://hdl.handle.net/10458/5983.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Yuya. “Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy.” 2017. Web. 18 Jan 2019.
Vancouver:
Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi Y. Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy. [Internet] [Thesis]. University of Miyazaki / 宮崎大学; 2017. [cited 2019 Jan 18].
Available from: http://hdl.handle.net/10458/5983.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi Y. Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy. [Thesis]. University of Miyazaki / 宮崎大学; 2017. Available from: http://hdl.handle.net/10458/5983
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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Open Access Theses and Dissertations