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Gardner, Samantha. "Gonadotropin-releasing hormone targets Wnt signalling". Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29112.
Pełny tekst źródłaFlanagan, Colleen A. "Gonadotropin releasing hormone receptor ligand interactions". Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27029.
Pełny tekst źródła李繼仁 i Kai-yan Lee. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31214332.
Pełny tekst źródłaLee, Kai-yan. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus /". Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18038165.
Pełny tekst źródła顔秀慧 i S. W. Ngan. "Transcriptional regulation of the human gonadotropin releasing hormonereceptor gene". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240847.
Pełny tekst źródłaCronin, A. S. "Neurotrophic responses of developing Gonadotropin-releasing hormone neurons". Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598166.
Pełny tekst źródłaKirkpatrick, Bridgette Lee 1966. "Hormonal regulation of gonadotropin releasing hormone receptor expression in the ewe". Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282660.
Pełny tekst źródłaNgan, S. W. "Transcriptional regulation of the human gonadotropin releasing hormone receptor gene /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21687584.
Pełny tekst źródłaChen, Junling. "Ligand-independent activation of steroid hormone receptors by gonadotropin-releasing hormone". Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/34980.
Pełny tekst źródłaSadie, Hanél. "Transcriptional regulation of the mouse gonadotropin-releasing hormone receptor gene in pituitary gonadotrope cell lines". Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/1495.
Pełny tekst źródłaGonadotropin-releasing hormone (GnRH), acting via its cognate receptor (GnRHR) is the primary regulator of mammalian reproductive function. Pituitary sensitivity to GnRH can be directly correlated with GnRHR levels on the surface of the pituitary gonadotrope cells, which can be regulated at transcriptional, post-transcriptional and post-translational levels. This study investigated mechanisms of transcriptional regulation of mouse GnRHR expression in two mouse gonadotrope cell lines, αT3-1 and LβT2, using a combination of endogenous mRNA expression studies, promoter-reporter studies, a two-hybrid protein-protein interaction assay, Western blotting, and in vitro protein-DNA binding studies. In the first part of the study, the role of two GnRHR promoter nuclear receptor binding sites (NRSs) and their cognate transcription factors in basal and Protein Kinase A (PKA)-stimulated regulation of GnRHR promoter activity was investigated in αT3-1 cells. The distal NRS was found to be crucial for basal promoter activity in these cells. While the NRSs were not required for the PKA response in these cells, results indicate a modulatory role for the transcription factors Steroidogenic Factor-1 (SF-1) and Nur77 via these promoter elements. The second part of the study focused on elucidating the mechanism of homologous regulation of GnRHR transcription in LβT2 cells, with a view to defining the respective roles of PKA and Protein Kinase C (PKC) in the transcriptional response to GnRH. In addition, the respective roles of the NRSs, the cyclic AMP response element (CRE) and the Activator Protein-1 (AP-1) promoter cis elements, together with their cognate transcription factors, in basal and GnRH-stimulated GnRHR promoter activity, were investigated. Homologous upregulation of transcription of the endogenous gene was confirmed, and was quantified by means of real-time RTPCR. The GnRH response of the endogenous gene and of the transfected promoter-reporter construct required PKA and PKC activity, and the GnRH response of the promoter-reporter construct was found to be dependent on a functional AP-1 site. Furthermore, GnRH treatment resulted in increased binding of phosphorylated cAMP-response element binding protein (phospho-CREB) and decreased expression and binding of SF-1 to their cognate cis elements in vitro, and stimulated a direct interaction between SF-1 and CREB, suggesting that these events are also required for the full transcriptional response to GnRH. This study is the first providing detail regarding the mechanism of transcriptional regulation of GnRHR expression in LβT2 cells by GnRH. Based on results from this study, a model has been proposed which outlines for the first time the kinase pathways, the promoter cis elements and the cognate transcription factors involved in homologous regulation of GnRHR transcription in the LβT2 cell line. As certain aspects of this model have been confirmed for the endogenous GnRHR gene, the model is likely to be physiologically relevant, and provides new ideas and hypotheses to be tested in future studies.
Kang, Sung Keun. "Role of gonadotropin-releasing hormone in the ovarian cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0020/NQ56568.pdf.
Pełny tekst źródłaStavrou, Emmanouil. "Regulation of FOXO transcription factors by gonadotropin-releasing hormone". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5686.
Pełny tekst źródłaNelson, Shelley B. "Neuron-specific regulation of the gonadotropin-releasing hormone gene /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9951423.
Pełny tekst źródłaVan, Biljon Wilma. "The mammalian type II gonadotropin-releasing hormone receptor : cloning, distribution and role in gonadotropin gene expression". Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/17333.
Pełny tekst źródłaENGLISH ABSTRACT: Gonadotropin-releasing hormone (GnRH) is well known as the central regulator of the reproductive system through its stimulation of gonadotropin synthesis and release from the pituitary via binding to its specific receptor, known as the gonadotropin-releasing hormone receptor type I (GnRHR-I). The gonadotropins, luteinising hormone (LH) and follicle-stimulating hormone (FSH), bind to receptors in the gonads, leading to effects on steroidogenesis and gametogenesis. The recent finding of a second form of the GnRH receptor, known as the type II GnRHR or GnRHR-II, in non-mammalian vertebrates triggered the interest into the possible existence and function of a GnRHR-II in humans. The current study addressed this issue by investigating the presence of transcripts for a GnRHR-II in various human tissues and cells. While it was demonstrated that antisense transcripts for this receptor, containing sequence of only two of the three coding exons, are ubiquitously and abundantly expressed in all tissues examined, potentially full-length (containing all three exons), sense transcripts for a GnRHR-II were detected only in human ejaculate. Further analysis revealed that the subset of cells in the ejaculate expressing these transcripts is mature sperm. These findings, together with the reported role for GnRH in spermatogenesis and reproduction led to the further analysis of the presence of a local GnRH/GnRHR network in human and vervet monkey ejaculate or sperm. Indeed, such a network seems to be present in humans since transcripts for both forms of GnRH present in mammals, as well as transcripts for the GnRHR-I, are expressed in human ejaculate. Furthermore, transcripts for the GnRHR-II are expressed in both human and vervet monkey ejaculate. Thus, it would appear that locally produced GnRH-1 and/or GnRH-2 in the human male reproductive tract might mediate their effects on fertility via a local GnRHR-I, and possibly via GnRHR-II. Remarkably, in the pituitary, LH and FSH are present in the same gonadotropes, yet they are differentially regulated by GnRH under various physiological conditions. While it is well established that post-transcriptional regulatory mechanisms occur, the contribution of transcriptional regulation to the differential expression of the LHβ- and FSHβ-subunit genes is unclear. In this study, the role of GnRH-1 and GnRH-2 via the GnRHR-I and the GnRHR-II in transcriptional regulation of mammalian LHβ- and FSHβ genes was determined in the LβT2 mouse pituitary gonadotrope cell-line. It is demonstrated for the first time that GnRH-1 may affect gonadotropin subunit gene expression via GnRHR-II in addition to GnRHR-I, and that GnRH-2 also has the ability to regulate gonadotropin subunit gene expression via both receptors. Similar to other reports, it is shown that the transcriptional response to GnRH-1 of LHβ and FSHβ is low (about 1.4-fold for bLHβLuc and 1.2-fold for oFSHβLuc). In addition, evidence is supplied for the first time that GnRH-2 transcriptional regulation of the gonadotropin β subunits is also low (about 1.5-fold for bLHβLuc and 1.1-fold for oFSHβLuc). It is demonstrated that GnRH-1 is a more potent stimulator of bLHβ promoter activity as compared to GnRH-2 via the GnRHR-I, yet both hormones result in a similar maximum induction of bLHβ. However, GnRH-2 is a more efficacious stimulator of bLHβ transcription via the GnRHR-II than GnRH-1. No discriminatory effect of GnRH-1 vs. GnRH-2 was observed for oFSHβ promoter activity via GnRHR-I or GnRHR-II. By comparison of the ratio of expression of transfected oFSHβ- and bLHβ promoterreporters via GnRH-1 with that of GnRH-2, it is shown that GnRH-2 is a selective regulator of FSHβ gene transcription. This discriminatory effect of GnRH-2 is specific for GnRHR-I, as it is not observed for GnRHR-II, where GnRH-1 results in a greater oFSHβ- to-bLHβ ratio. These opposite selectivities for GnRHR-I and GnRHR-II on the ratios of oFSHβ:bLHβ promoter activity for GnRH-1 vs. GnRH-2 suggest a mechanism for fine control of gonadotropin regulation in the pituitary by variation of relative GnRHR-I vs. GnRHR-II levels. In addition, a concentration-dependent modulatory role for PACAP on GnRH-1- and GnRH-2-mediated regulation of bLHβ promoter activity, via both GnRHR-I and GnRHR-II, and of oFSHβ promoter activity, via GnRHR-I, is indicated. The concentration-dependent effects suggest the involvement of two different signalling pathways for the PACAP response. Together these findings suggest that transcription of the gonadotropin genes in vivo is under extensive hormonal control that can be finetuned in response to varying physiological conditions, which include changing levels of GnRH-1, GnRH-2, GnRHR-I and GnRHR-II as well as PACAP.
AFRIKAANSE OPSOMMING: Gonadotropien-vrystellingshormoon (GnRH) is bekend as die sentrale reguleerder van die voorplantingsisteem deur die stimulasie van gonadotropiensintese en - vrystelling vanaf die pituïtêre klier via binding aan ‘n spesifieke reseptor, die sogenaamde tipe I gonadotropien-vrystellingshormoonreseptor (GnRHR-I). Die gonadotropiene, lutineringshormoon (LH) en follikel-stimuleringshormoon (FSH), bind aan reseptore in die gonades waar dit steroïedogenese en gametogenese beïnvloed. Die onlangse ontdekking van ‘n tweede vorm van die GnRH-reseptor, bekend as die tipe II GnRHR of GnRHR-II, in nie-soogdier vertebrate het belangstelling in die moontlike bestaan en funksie van ‘n GnRHR-II in die mens gewek. Hierdie kwessie is aangeraak deur die teenwoordigheid van transkripte vir ‘n GnRHR-II in verskeie weefsel- en seltipes van die mens te ondersoek. Daar is aangetoon dat nie-sin transkripte vir hierdie reseptor, wat die DNA-opeenvolgings van slegs twee van die drie koderende eksons bevat het, oormatig uitgedruk word in al die weefseltipes wat ondersoek is. Daarteenoor is potensieel vollengte (bevattende al drie eksons) sin transkripte vir ‘n GnRHR-II in die mens slegs in semen gevind. Verdere analise het getoon dat dit volwasse sperma binne die semen is wat laasgenoemde transkripte uitdruk. Hierdie bevindinge, tesame met die aangetoonde rol vir GnRH in spermatogenese en reproduksie het gelei tot die verdere analise van die teenwoordigheid van ‘n lokale GnRH/GnRHR-netwerk in mens- en blouaapsemen of -sperm. So ‘n netwerk blyk om teenwoordig te wees in die mens, aangesien transkripte vir beide vorme van GnRH wat in soogdiere gevind word, asook transkripte vir die GnRHR-I, in menssemen uitgedruk word. Daarbenewens word transkripte vir die GnRHR-II uitgedruk in beide mens- en blouaapsemen. Dit wil dus voorkom asof lokaalgeproduseerde GnRH-1 en/of GnRH-2 in die manlike voortplantingstelsel van die mens hul effek op vrugbaarheid bemiddel via ‘n lokale GnRHR-I, en moontlik ook via GnRHR-II. Dit is opmerklik dat LH en FSH teenwoordig is in dieselfde gonadotroopselle van die pituïtêre klier en tog verskillend gereguleer word deur GnRH tydens verskeie fisiologiese kondisies. Terwyl dit bekend is dat post-transkripsionele reguleringsmeganismes teenwoordig is, is die bydrae van transkripsionele regulering tot die differensiële uitdrukking van die LHβ- en FSHβ-subeenheidgene minder duidelik. In hierdie studie is die rol van GnRH-1 en GnRH-2 via die GnRHR-I en die GnRHR-II in transkripsionele regulering van soogdier-LHβ- en -FSHβ-gene in die LβT2 muis pituïtêre gonadotroopsellyn bepaal. Dit is vir die eerste keer aangetoon dat GnRH-1 ‘n effek mag hê op gonadotropiensubeenheid-geenuitdrukking via GnRHR-II bykomend tot GnRHR-I, en dat GnRH-2 ook die vermoë besit om gonadotropiensubeenheid-geenuitdrukking via beide reseptore te reguleer. Soos deur ander studies aangetoon is die transkripsionele respons van LHβ en FSHβ tot GnRH-1 klein (ongeveer 1.4-voudig vir bLHβLuc en 1.2- voudig vir oFSHβLuc). Verder is daar vir die eerste keer bewys gelewer dat transkripsionele regulering van die gonadotropien β-subeenhede deur GnRH-2 ook gering is (ongeveer 1.5-voudig vir bLHβLuc en 1.1-voudig vir oFSHβLuc). Daar is aangetoon dat GnRH-1 ‘n sterker stimuleerder van bLHβ-promotoraktiwiteit is in vergelyking met GnRH-2 via die GnRHR-I, hoewel beide hormone tot ‘n soortgelyke maksimum induksie van bLHβ lei. GnRH-2 is egter ‘n meer effektiewe stimuleerder van bLHβ-transkripsie as GnRH-1 via die GnRHR-II. Geen verskille is gevind tussen die effekte van GnRH-1 en GnRH-2 op oFSHβ-promotoraktiwiteit via GnRHR-I of GnRHR-II nie. Wanneer die verhouding van uitdrukking van getransfekteerde oFSHβ- en bLHβ- promotor-verslaggewers via GnRH-1 met dié van GnRH-2 vergelyk is, is aangetoon dat GnRH-2 ‘n selektiewe reguleerder van FSHβ-geentranskripsie is. Hierdie diskriminasieeffek van GnRH-2 is spesifiek vir GnRHR-I aangesien dit nie vir GnRHR-II waargeneem word nie. GnRH-1 lei tot ‘n groter oFSHβ tot bLHβ-verhouding via GnRHR-II. Hierdie teenoorgestelde selektiwiteite van GnRHR-I en GnRHR-II op die verhoudings van oFSHβ tot bLHβ-promotoraktiwiteit vir GnRH-1 teenoor GnRH-2 suggereer dat daar ‘n meganisme bestaan vir die fyn regulering van gonadotropiene in die pituïtêre klier, deurdat die relatiewe vlakke van GnRHR-I teenoor GnRHR-II gevarieer word. Daarbenewens is ‘n konsentrasie-afhanklike moduleringsrol vir PACAP op GnRH-1- en GnRH-2-bemiddelde regulering van bLHβ-promotoraktiwiteit aangetoon, via beide GnRHR-I en GnRHR-II, asook op oFSHβ-promotoraktiwiteit via GnRHR-I. Hierdie konsentrasie-afhanklike effekte dui op die betrokkenheid van twee verskillende seinpadweë vir die PACAP-respons. Tesame suggereer hierdie bevindinge dat transkripsie van die gonadotropiengene in vivo onder ekstensiewe hormonale kontrole is wat verfyn kan word in respons to veranderlike fisiologiese kondisies. Laasgenoemde sluit veranderende vlakke van GnRH-1, GnRH-2, GnRHR-I en GnRHR-II asook PACAP in.
Powell, R. C. "Evolution of the structure and function of vertebrate brain gonadotropin-releasing hormone". Master's thesis, University of Cape Town, 1986. http://hdl.handle.net/11427/27201.
Pełny tekst źródłaWibullaksanakul, Sunee. "Regulation of gonadotropin releasing hormone (GnRH) secretion : in-vitro studies in the male rat". Thesis, The University of Sydney, 1992. https://hdl.handle.net/2123/26487.
Pełny tekst źródłaNicola, Angela Cristina de. "Atividade dos neurônios noradrenérgicos do Locus coeruleus e o conteúdo de GnRH em ratas Wistar acíclicas /". Araçatuba, 2013. http://hdl.handle.net/11449/92094.
Pełny tekst źródłaCo-orientador: Janete Aparecida Anselmo-Franci
Banca: Maristela de Oliveira Poletini
Banca: Jacqueline Nelisis Zanoni
Resumo: As alterações nos componentes reprodutivos do eixo hipotálamo-hipófise-gônadas em muitas fêmeas de mamíferos determinam a transição gradual de ciclos reprodutivos regulares para ciclos irregulares, com perda de fertilidade. A interação dos neurônios do hormônio liberador de gonadotrofinas (GnRH) e esteróides gonadais representa função chave na neurobiologia do envelhecimento, pois a sobreposição temporal da senescência endócrina e neural está mecanicamente interligada pelas alças de retroalimentação. Estímulos do locus coeruleus (LC) para a área pré-óptica (APO) e eminência mediana são essenciais para a liberação das gonadotrofinas e seus neurônios apresentam receptores para estrógeno e progesterona, sugerindo controle dos esteróides ovarianos. Neste estudo foi avaliado a atividade de células neuronais localizadas em áreas e núcleos envolvidos com o controle de ação dos neurônios GnRH de ratas Wistar no período de transição para a aciclicidade. Para este trabalho foram utilizadas fêmeas Wistar cíclicas (4 meses) e acíclicas (18-20 meses) submetidas à decapitação ou perfusão às 10, 14 e 18 h na fase do diestro. Após serem retirados, os cérebros dos animais decapitados foram congelados e armazenados para posterior determinação do conteúdo de GnRH hipotalâmico e do conteúdo de noradrenalina e dopamina na APO. Os cérebros perfundidos foram cortados seriadamente em secções coronais de 30 μm para a APO e o LC e...
Abstract: Changes in reproductive components of the hypothalamic-pituitary-gonadal axis in many female mammals determine the gradual transition from regular reproductive cycles to irregular cycles, with loss of fertility. The interaction of neurons of gonadotropin-releasing hormone (GnRH) and gonadal steroids represents key role in the neurobiology of aging, because the temporal overlap of endocrine and neural senescence is mechanically interconnected by feedback loops. Stimulation of the locus coeruleus (LC) for the preoptic area (POA) and median eminence are essential for the release of gonadotropins and their neurons have receptors for estrogen and progesterone, suggesting control of ovarian steroids. Therefore, in this study we evaluated the activity of neuronal cells located in areas and nuclei involved in the control of action of GnRH neurons of female rats during the transition to acyclicity. For this study, we used cyclic female (4 months) and acyclic (18-20 months) rats underwent perfusion or decapitation at 10, 14 and 18 h of diestrus day. The brains from decapitated animals, after removed, were frozen and stored for subsequent determination of the hypothalamic GnRH content and the noradrenaline and dopamine content in the POA. The perfused brains were serially cut into coronal sections of 30 μm to POA and LC and subsequently submitted to immunohistochemical labeling for Fos (FRA) and FRA / TH, respectively. For quantitative analysis of the POA were considered plates containing AVPe being the counting of neurons FRA-ir performed from the insertion of the box with...
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Von, Boetticher S. "Investigating the mechanism of transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by dexamethasone". Thesis, Link to the online version, 2008. http://hdl.handle.net/10019/1796.
Pełny tekst źródłaPepa, Patricia Ann. "Repression of gonadotropin-releasing hormone gene expression by androgen receptor". Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/fullcit?p1477926.
Pełny tekst źródłaTitle from first page of PDF file (viewed July 16, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (leaves 59-62).
Cheng, Kwai Wa. "Transcription regulation of human gonadotropin-releasing hormone receptor gene expression". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61070.pdf.
Pełny tekst źródłaMiller, Nichol L. G. "Transcriptional control of the gonadotropin-releasing hormone gene in development". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC IP addresses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3296836.
Pełny tekst źródłaTitle from first page of PDF file (viewed June 3, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 113-126).
Ford, H. "Regulation of gonadotropin-releasing hormone neurons by the neurotransmitter glutamate". Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599110.
Pełny tekst źródłaCheung, Wai-ting. "Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41634184.
Pełny tekst źródłaFernandes, S. M. (Sandra Maria). "Transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by glucocorticoids". Thesis, Stellenbosch : Stellenbosch University, 2007. http://hdl.handle.net/10019.1/19595.
Pełny tekst źródłaENGLISH ABSTRACT: The gonadotropin-releasing hormone (GnRH) receptor is a G-protein-coupled receptor in the pituitary gonadotropes and is an important control point for reproduction. GnRH binds to the GnRH receptor (GnRHR) resulting in the synthesis and release of follicle stimulating hormone (FSH) and luteinizing hormone (LH). The sensitivity of the pituitary to GnRH can be directly correlated with GnRHR levels. The mouse GnRHR promoter contains three cis elements containing binding sites for steroidogenic factor-1 (SF-1), namely site 1 (-15/-7), site 2 (-244/- 236) and site 3 (-304/-296) as well as an activator protein-1 (AP-1)-like consensus sequence (TGAGTCA) at position –336/-330. While sites 1 and 2 and the AP-1 site have been previously shown to be involved in regulation of transcription of the mouse GnRHR (mGnRHR) promoter in some cell lines, the role of site 3 has not been previously investigated. This study investigated whether transcription of the mGnRHR gene is regulated by GnRH and glucocorticoids in the LβT2 gonadotrope pituitary cell line, and the role therein of site 3 and the AP-1 site and their cognate proteins, using a combination of in vitro protein- DNA binding studies and promoter-reporter assays. The role played by site 3 and the AP-1 site in basal transcription of the mGnRHR gene in LβT2 cells was the first area of investigation during this study. Luciferase reporter plasmids containing 600 bp of the mGnRHR promoter were used where the site 3 and AP-1 sites were either wild-type or mutated. Two constructs were prepared from the wild-type construct, i.e. wild type (LG), site 3 mutant (m3) and AP-1 mutant (mAP-1). Transfection of LG, m3 and mAP-1 plasmids into LβT2 cells was carried out to determine the effect of these mutations on the basal expression of the mGnRHR gene. Mutation of site 3 resulted in a 1.5 fold increase in the transcriptional activity of the mGnRHR promoter. This suggests that site 3 plays a role in the inhibition of basal transcriptional levels of the mGnRHR promoter in LβT2 cells. Mutation of the AP-1 site resulted in a 50% decrease in basal transcriptional levels of the mGnRHR promoter in LβT2 cells. This suggests that the AP-1 site is involved in positively mediating the basal transcriptional response of the GnRHR promoter in LβT2 cells. Experiments towards the understanding of the mechanism of the cis elements (site 3 and AP-1 site) on the mGnRHR promoter were carried out along with the role of protein kinase A (PKA) pathways, proteins involved and the effect of varying doses for varying times of GnRH, as well as the overexpression of PKA and the SF-1 protein. It was found that site 3 and the AP-1 site are not involved in the GnRH response. Results suggest that site 3 is partially involved in the PKA response in LβT2 cells. Site 3 can bind SF-1 protein as shown via competitive electrophoretic mobility shift assays (EMSA). When EMSA’s were performed on the AP-1 site the findings were that the c-Fos protein was not involved in the activation of the AP-1 site. A factor was found to bind to the AP-1 site, which did not require the intact AP-1 site, suggesting that it could be the c-Jun protein that binds to the AP-1 site under basal conditions. Another area that was investigated was whether the mGnRHR promoter can be regulated by dexamethasone (dex) either via the AP-1 site or site 3. A dose and time-dependent increase in promoter activity was observed with dex. This effect appears to require site 3 and the AP-1 site, as shown by the complete loss of response when these sites were individually mutated, consistent with a functional interaction between site 3 and the AP-1 site in LβT2 cells.
AFRIKAANSE OPSOMMING: Die gonadotropienvrystellings hormoon (GnRH) reseptor is ‘n G-proteïen-gekoppelde reseptor in die pituitêre gonadotrope en is ’n belangrike beheerpunt vir reproduksie. GnRH bind aan die GnRH reseptor (GnRHR) met die gevolg dat follikel stimulerende hormoon (FSH) en luteïeniserende (LH) gesintetiseer en vrygestel word. Die sensitiwiteit van die pituitêre klier vir GnRH kan direk met GnRHR vlakke gekorreleer word. Die muis GnRHR promotor bevat drie cis elemente met bindingssetels vir steroïedogeniese faktor 1 (SF1), naamlik setel 1 (-15/-7), setel 2 (-244/-236) en setel 3 (-304/-296) sowel as ’n aktiveerder proteïen 1 (AP-1) tipe konsensus sekwens (TGAGTCA) in posisie -336/-330. Terwyl setels 1 en 2 en die AP-1 setel voorheen getoon is om by die regulering van transkripsie van die muis GnRHR (mGnRHR) promotor in party sellyne betrokke te wees, is die rol van setel 3 nog nie vantevore bestudeer nie. In hierdie studie is ondersoek of die transkripsie van die mGnRHR geen deur GnRH en glukokortikoïede in die LβT2 gonadotroop pituitêre sellyn gereguleer word, en die rol van setel 3 en die AP-1 setel en hulle binders, deur gebruik te maak van in vitro proteïen-DNA bindings studies en promotor-verslaggewer essais. Die rol wat setel 3 en die AP-1 setel in basale transkripsie van die mGnRHR gene in LβT2 selle gespeel het, was die eerste onderwerp wat in hierdie studie bestudeer is. Lusiferase verslaggewer plasmiede wat die eerste 600 bp van die mGnRHR promotor bevat het en waarin setel 3 en die AP-1 setels óf wilde tipe óf gemuteer was, is gebruik. Two konstrukte is vanaf die wilde tipe konstruk berei, naamlik wilde tipe (LG), ’n setel 3 mutant (m3) en ’n AP-1 mutant (mAP-1). Transfeksie van LG, m3 en mAP-1 plasmiede in LβT2 selle is deurgevoer om te bepaal wat die effek van hierdie mutasies op die basale ekspressie van die mGnRHR gene was. Mutasie van setel 3 het ’n 1.5-voudige toename in die transkripsionele aktiwiteit van die mGnRHR promotor tot gevolg gehad. Dit suggereer dat setel 3 ’n rol in die inhibisie van die basale transkripsievlakke van die mGnRHR promotor in LβT2 selle speel. Mutasie van die AP-1 setel het tot ‘n 50% verlaging in basale transkripsievlakke van die mGnRHR promotor in LβT2 selle gelei. Dit suggereer dat die AP-1 setel betrokke is in die positiewe bemiddeling van die basale transkriptionele respons van die GnRHR promotor in LβT2 selle. Eksperimente wat gemik was om die meganisme van die cis-elemente (setel 3 en die AP-1 setel) op die mGnRHR promotor te verklaar, asook om die rol van proteïen kinase A (PKA) paaie, proteïene daarby betrokke en die effek van varieende dosisse vir verskillende tye van GnRH, sowel as die oorekspressie van PKA en die SF-1 proteïen, is deurgevoer. Dit is gevind dat setel 3 en die AP-1 setel nie betrokke by die GnRH respons is nie. Die resultate suggereer dat setel 3 gedeeltelik betrokke is by die PKA respons van LβT2 selle. Setel 3 kan SF-1 proteïen bind soos getoon deur kompeterence elektroforetiese mobiliteits verskuiwings essais (EMSA). As EMSA’s deurgevoer is op die AP-1 setel is bevind dat die c-Fos proteïen nie betrokke is in die aktivering van die AP-1 setel nie. ’n Faktor is gevind om aan die AP-1 setel te bind wat nie ’n intakte AP-1 setel vereis het nie, wat gesuggereer het dat dit die c-Jun proteïen kan wees wat aan die AP-1 setel onder basale omstandighede bind. ’n Ander area wat ondersoek is, is of die GnRHR promotor gereguleer kan word deur deksametasoon (dex) óf via die AP-1 setel óf via setel 3. ’n Dosis en tyds-afhanklike toename in promotor aktiwiteit is waargeneem met dex. ’n Vereiste vir hierdie effek blyk om die teenwoordigheid van setel 3 en die AP-1 setel te wees, soos aangetoon deur die totale verlies aan response as hierdie twee setels individueel gemuteer is, en wat weereens in ooreenstemming met die funksionele interaksie tussen setel 3 en die AP-1 setel in LβT2 selle is.
Clarkson, Jenny, i n/a. "Activation of Gonadotropin-releasing hormone neurons by Kisspeptin in the mouse". University of Otago. Department of Physiology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081208.114143.
Pełny tekst źródłaMaze, Timothy D. "Development of the induced gonadotropin surge mechanism in the prepubertal heifer". Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2525.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains viii, 71 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 61-70).
Cheung, Wai-ting, i 張慧婷. "Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41634184.
Pełny tekst źródłaHoo, L. C., i 何麗莊. "Transcriptional regulation of the human gonadotropin-releasing hormone(GnRH) II and GnRH receptor genes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29297011.
Pełny tekst źródłaMa, Chi-him Eddie. "Molecular studies of gonadotropin releasing hormone receptors and estrogen receptors in goldfish (Carassius auratus)". Click to view the E-thesis via HKUTO, 2000. http://sunzi.lib.hku.hk/hkuto/record/B4257531X.
Pełny tekst źródła馬智謙 i Chi-him Eddie Ma. "Molecular studies of gonadotropin releasing hormone receptors and estrogen receptors in goldfish (Carassius auratus)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B4257531X.
Pełny tekst źródłaMorton, Stephanie. "Effects of continuous treatment with gonadotropin-releasing hormone during the anovulatory season on gonadotropin secretion, follicular dynamics and ovulation in the mare". Texas A&M University, 2004. http://hdl.handle.net/1969.1/1551.
Pełny tekst źródłaVasilyev, Vyacheslav V. "Regulation of gonadotropin [beta]-subunit gene expression by gonadotropin-releasing hormone in immortalized pituitary cell lines /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2001. http://wwwlib.umi.com/cr/ucsd/fullcit?p3022216.
Pełny tekst źródłaEly, Heather Ashlie. "A mechanism for gonadotropin-releasing hormone induction of c-Fos gene expression in pituitary gonadotrope cells". Diss., [La Jolla, Calif.] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1462104.
Pełny tekst źródłaTitle from first page of PDF file (viewed March 19, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 66-72).
戚賜聰 i Chi-chung Stanley Chik. "Characterization of two chicken gonadotropin releasing hormone-II genes in goldfish, Carassius Auratus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31220629.
Pełny tekst źródłaBinder, April Kay. "The role of ß-catenin in the gonadotrope transcriptional network interactions with SF1 and TCF /". Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Dissertations/Fall2009/a_binder_090309.pdf.
Pełny tekst źródłaLee, King-yiu. "Molecular cloning and characterization of gonadotropin-releasing hormone receptors in the black seabream (Mylio macrocephalus)". Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22823876.
Pełny tekst źródłaVon, Schalburg Kristian Robert. "The gonadotropin-releasing hormone gene : characterization, regulation and expression in two salmonids". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ36651.pdf.
Pełny tekst źródłaMirhadi, Eila. "Regulation of gonadotropin-releasing hormone (GnRH) transcript production in the goldfish ovary". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ38601.pdf.
Pełny tekst źródłaRonacher, Katharina. "Internalisation of the type II gonadotropin-releasing hormone receptor of marmoset monkey". Doctoral thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/8599.
Pełny tekst źródłaThe mammalian type II GnRH receptor has a C-terminal tail unlike the mammalian type I GnRH receptor, which uniquely lacks the cytoptasmic C- terminal domain. lnternalisation of a mammalian type ll GnRH receptor has never been investigated, therefore this thesis studies the internalisation pathway of the type ll GnRH receptor. As the C-terminal tail mediates rapid internalisation of many G protein-coupled receptors this research investigates the functional role of the C-terminal tail and intracellular loop in receptor internalisation. The internalisation pathway of the type ll GnRH receptor in COS-1 cells was investigated by co expressing dominant negative mutants and wild- type constructs of G protein-coupled receptor kinases (GRKs), dynamin-1 and β-arrestin 1 and 2 with the type II GnRH receptor. The results show that internatisation of the receptor requires GRK 2 and dynamin but does not require β-arrestin 1 and 2. Furthermore, inhibitors to both the caveolae pathway as well as the clathrin coated vesicle endocytosis abolished receptor internalisation indicating that both structures are involved in internalisation of the receptor. Even though in COS-1 cells the type ll GnRH receptor internatises in a β-arrestin independent manner, internalisation of this receptor can be enhanced by over-expression of wild type β-arrestin. This indicates that the type ll GnRH receptor is able to utilise a β-arrestin mediated internaltsation pathway if high levels of β-arrestin are present in the cell. The mammalian type ll GnRH receptor internalises with enhanced rate and extent compared to the tail-less human type I GHRH receptor. The role of the C-terminal tail of the type ll GnRH receptor in internalisation was investigated by measuring internalisation of C-terminally truncated mutants. It was found that the region between Gly 343 and Ser 335 within the C-terminal domain is important for receptor internalisation. Substitution of putative phosphorylation sites within this region revealed that Ser 338 and Ser 339 are critical for rapid receptor internalisation. Furthermore a serine residue in intracellular loop three (Ser 251) was shown to play a role in signalling as well as in internalisation. Since dominant negative GRK 2 could not inhibit internalisation of a mutant lacking all three serine residues, but could reduce internalisation of the wild-type receptor, we suggest that Ser 251, 338 and 339 are target of phosphorylation by GRK. However these phosphorylation sites as well as the C-terminal tail are not necessary for β-arrestin dependent internalisation. Taken together this thesis elucidates the internalisation pathway of a mammalian type lI GnRH receptor and identified residues within the C-terminal tail and intracellular loop three that are critical for rapid internalisation.
Pithey, Anne Louise. "Autocrine regulation of gonadotropin-releasing hormone in immortalized hypothalamic GT1-7 neurons". Master's thesis, University of Cape Town, 1994. http://hdl.handle.net/11427/27030.
Pełny tekst źródłaHutchinson, Emerentia. "The cloning of novel gonadotropin-releasing hormone receptors by polymerase chain reaction". Master's thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26968.
Pełny tekst źródłaMacConell, Leigh Anne. "The regulation of gonadotropin-releasing hormone biosynthesis and release by activin A /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9904817.
Pełny tekst źródłaKelley, Carolyn Griffith. "Neuron-specific transcriptional activators directing expression of the gonadotropin-releasing hormone gene /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9984304.
Pełny tekst źródłaGivens, Marjory L. "Molecular mechanisms promoting neuron-restricted expression of the gonadotropin-releasing hormone gene /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3129941.
Pełny tekst źródłaChik, Chi-chung Stanley. "Characterization of two chicken gonadotropin releasing hormone-II genes in goldfish, Carassius Auratus : y Chik Chi Chung Stanley". Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2056630X.
Pełny tekst źródłaMiles, Lauren E. C. "Mammalian cell growth and proliferation mediated by the gonadotropin-releasing hormone (GnRH) receptor : role of novel interacting protein partners". University of Western Australia. Centre for Medical Research, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0090.
Pełny tekst źródłaHe, Mulan, i 何木蘭. "Molecular studies of two functional gonadotropin-releasing hormone receptors in goldfish, Carassius auratus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240240.
Pełny tekst źródła曾美好 i May-ho Tsang. "Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) secretion and gene expression in a GnRH neuronal cell line". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31213698.
Pełny tekst źródłaTsang, May-ho. "Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) secretion and gene expression in a GnRH neuronal cell line /". Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17095219.
Pełny tekst źródłaWormald, Patricia J. "GnRH and neuropeptide regulation of gonadotropin secretion from cultured human pituitary cells". Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27168.
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