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1
Sun, Yuh-Man. "Cloning and charaterisation of the Thyrotrophin-releasing hormone receptor and Gonadotrophin-relasing hormone receptor from chicken pituitary gland". Doctoral thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26973.
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The hypothalamic hormones, thyrotrophin-releasing hormone (TRH) and gonadotrophin-releasing hormone (GnRH), play pivotal roles in the growth and sexual maturation of chickens. In chickens, TRH regulates the release and synthesis of thyrotrophin (TSH) and also acts as a growth hormone-releasing factor. GnRH stimulates the release and synthesis of gonadotrophins (LH and FSH). TRH and GnRH are released and stored in the median eminence, and both hormones are transported into the pituitary gland via the hypophysial portal circulation. TRH and GnRH exert their physiological functions by binding to their specific receptors (TRH receptor and GnRH receptor, respectively) on the surface of cells in the pituitary gland. The activated receptors couple to guanine nucleotide-binding regulatory proteins (G proteins), Gq and/or G11, which in turn triggers the secondary messenger [1,2- diacylglycerol (DAG) and inositoltrisphosphate (IP3)] signalling cascade. The signalling generates the physiological effects of the hormones. The TRH-R and GnRH-R are members of G-protein coupled receptor (GPCR) family. The objective of this thesis was to clone and characterise the chicken TRH and GnRH receptors as useful tools for investigating the regulatory roles of TRH and GnRH receptors in the growth and sexual maturation of chickens. In addition, sequence information of the receptors would potentially assist in elucidating the binding sites and the molecular nature of the processes involved in receptor activation.
2
Dromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.
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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
3
Kaur, Baljit. "The conformational analysis of thyrotropin releasing hormone and its analogues". Thesis, Manchester Metropolitan University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284878.
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Ouafik, L'Houcine. "Etude sur la biosynthèse de la Thyrotropin-Releasing Hormone (TRH) pancréatique". Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37608585w.
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Ouafik, L'Houcine. "Etude sur la biosynthèse de la thyrotropin-releasing hormone (TRH) pancréatique". Aix-Marseille 2, 1987. http://www.theses.fr/1987AIX22004.
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Xiang, Shi Zhan. "Central control of the rat thyroid axis". Thesis, Brunel University, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320216.
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7
Chen, Junling. "Ligand-independent activation of steroid hormone receptors by gonadotropin-releasing hormone". Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/34980.
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Nuclear receptors including estrogen receptors (ERs) and progesterone receptors (PRs) are
activated by their ligands as well as by signaling pathways in response to peptide hormones and growth factors. In gonadotrophs, gonadotropin releasing hormones (GnRHs) act via the GnRH receptor (GnRHR). Both GnRH-I and GnRH-II activate an estrogen response element (ERE)-driven luciferase reporter gene in LβT2 mouse pituitary cells, and GnRH-I is more potent in this regard. The ERα is phosphorylated at Ser¹¹⁸ in the nucleus and at Ser¹⁶⁷ in both nucleus and cytoplasm after GnRI-I treatments, and this coincides with increased ERct binding to its co-activator, the P300/CBP-associated factor (PCAF). Most importantly, both GnRH subtypes robustly up-regulate expression of the immediate early response gene, Fosb, while co-treatment with ERα siRNA or PCAF siRNA attenuates this effect. This appears to occur at the transcriptional level because co-recruitment of ERα and PCAF to an ERE within the endogenous Fosb promoter is increased by GnRH treatments, as shown by chromatin
immunoprecipitation assays. Furthermore, cross-talk between GnRH-I and PR accentuates
gonadotropin production. GnRH-I activates a progesterone response element (PRE)-driven
luciferase reporter gene and gonadotropin a subunit (Gsua) gene expression in two mouse
gonadotroph cell lines, αT3-1 and LβT2. Up-regulation of the PRE-luciferase reporter gene
by GnRH-I is attenuated by pre-treatment with protein kinase A (H89) and protein kinase C
(GF109203X) inhibitors, while only GF109203X inhibits GnRH-1-induced Gsua mRNA levels. In both cell lines within the same time-frame, knockdown of PR levels by siRNA reduces GnRH-I activation of Gsua mRNA levels by approximately 40%. Both GnRH-I and GnRH-II also increase mouse Gnrhr-luciferase promoter activity and this is significantly
reduced by knockdown of PR in LβT2 cells. We conclude that the effects of GnRH-I on Fosb
and Gsua expression, as well as mouse Gnrhr promoter activity in mouse gonadotrophs are
mediated by ligand-independent activation of ERα and PR. These ligand-independent effects
of GnRHs on steroid hormone receptor function may influence the magnitude of changes in
the expression of specific genes in the pituitary during the mouse estrous cycle, which in this
context may serve as a model in the human menstrual cycle.
8
Ebiou, Jean-Claude. "Le rôle biologique de la thyrotropin-releasing hormone (TRH) dans le pancréas endocrine". Paris 7, 1992. http://www.theses.fr/1992PA077056.
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L'objectif de ce travail est la recherche du rôle biologique de la TRH pancréatique. La TRH a été initialement isolée de l'hypothalamus et caractérisée comme pGlu-His-ProNH₂. Elle a ensuite été détectée dans le pancréas endocrine désigne comme deuxième site de synthèse du peptide. La TRH est synthétisée à partir d'un précurseur de haut poids moléculaire. La maturation complète de celui-ci génèrerait 5 molécules de TRH, et 7 peptides de connexion. Nous avons montré que la TRH secrétée par le pancréas a les mêmes caractéristiques chromatographiques que le peptide synthétique. La sécrétion de la TRH pendant le développement est stimulé par le glucose et l'arginine, tandis que ces mêmes secretagogues inhibent la sécrétion chez l'adulte. Fait intéressant, la sécrétion de la TRH augmente avec l’âge, en dépit de la chute des contenus pancréatiques. Nous avons caractérise deux peptides de connexion de la prepro-TRH: prepro-TRH160-169 et prepro-TRH178-199, dans des ilots de Langerhans, et le prepro-TRH178-199 dans le milieu de sécrétion. Concernant le rôle biologique de la TRH pancréatique, nous avons montré que: la TRH exogène stimule la sécrétion basale du glucagon; l'immunoneutralisation de la TRH endogène secrétée par l'anticorps anti-TRH inhibe significativement la sécrétion du glucagon induite par l'arginine, la sécrétion de somatostatine est légèrement inhibée. Sur une fistule pancréatique, la TRH inhibe la sécrétion exocrine des protéines, bicarbonates, et du sodium. Les résultats préliminaires sur les cellules acinaires indiquent une absence d'effet TRH. L'effet TRH, observe in vivo, serait medié par le système nerveux central. Au cours du développement, la TRH n'a pas d'effet sur les secrétions d'insuline et glucagon. Nous pensons qu'elle agirait sur le processus de prolifération des cellules insulaires. La TRH stimule la sécrétion du glucagon des cellules alpha. Il serait intéressant de rechercher l'action biologique des deux peptides de connexion. La détermination du mécanisme d'action de la TRH pancréatique implique la caractérisation des sites de liaison spécifiques. Ce travail a été publié dans: Endocrinology 1992, 130(3):1371-1379; Endocrinology 1992, 131(2) (à paraitre en aout); prostate tumeurs 1991, (7):9-10 et 1992(9):6-7.
9
Ma, 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.
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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.
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Hart, G. R. "Mechanism of control of growth hormone release from the anterior pituitary : A role for thyrotropin-releasing hormone". Thesis, University of Sussex, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305765.
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Flanagan, Colleen A. "Gonadotropin releasing hormone receptor ligand interactions". Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27029.
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The decapeptide, gonadotropin releasing hormone (GnRH), is the central regulator of reproductive function. It binds to receptors on the gonadotrope cells of the pituitary and stimulates release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). Eleven different structural forms of GnRH have now been identified in various animal species. Chimaeric analogues of some of the variant forms of GnRH were synthesized in order to study the functional significance of the most common amino acid substitutions, which occur in positions 5, 7 and 8. Peptide binding affinities for sheep and rat GnRH receptors and potencies in stimulating LH and FSH release from cultured sheep pituitary cells and LH release from cultured chicken pituitary cells were measured. Histidine in position 5 decreased LH releasing potency in chicken cells, but slightly increased receptor binding affinity in rat and sheep membranes. Tryptophan in position 7 had minimal effect on GnRH activity in mammals, but increased LH release in chicken cells. Although differences in the structural requirements of mammalian and chicken GnRH receptors were anticipated, it was also found that rat GnRH receptors exhibited higher affinity for analogues with Tryptophan in position 7, than did sheep GnRH receptors. Substitutions in position 8 revealed the most marked differences in the structural requirements of mammalian and chicken GnRH receptors. Arginine was required for high GnRH activity in mammalian systems, but analogues with neutral substitutions in position 8 were more potent in chicken pituitary cells. The tolerance of position 8 substitutions, combined with the relatively small effects, in chicken cells, of incorporating a D-amino acid in position 6, indicate that the chicken GnRH receptor is less stringent than mammalian receptors in its recognition of peptide conformation. To examine how changes in ligand structure cause changes in receptor binding affinity and receptor activation, it was necessary to know the structures of the GnRH receptors. A protocol was developed for the purification of GnRH binding proteins from detergent-solubilized pituitary membranes, by affinity chromatography. This procedure yielded a protein which migrated as a single band on sodium dodecyl sulfate polyacrylamide gel electrophoresis, but was different from the recently cloned GnRH receptor. To test the proposal that the arginine residue in mammalian GnRH interacts with an acidic receptor residue, eight conserved acidic residues of the cloned mouse GnRH receptor were mutated to asparagine or glutamine. Mutant receptors were transiently expressed in COS-1 cells and tested for decreased preference for Arg⁸-containing ligands by ligand binding and inositol phosphate production. One mutant receptor, in which the glutamate residue in position 301 was mutated, exhibited decreased affinity for mammalian GnRH. The mutant receptor also exhibited decreased affinity for [Lys⁸]-GnRH, but unchanged affinity for [Gln⁸]-GnRH compared with the wildtype receptor, and increased affinity for the acidic analogue, [Glu⁸]-GnRH. This loss of affinity was specific for the residue in position 8, because the mutant receptor retained hiszh affinity for analogues with favourable substitutions in positions 5, 6 and 7. Thus, the Glu³⁰¹ residue of the GnRH receptor plays a role in receptor recognition of Arg⁸ in the ligand, consistent with an electrostatic interaction between these two residues. The Glu³⁰¹ and Arg⁸ residues were not required for the high affinity interactions of conformationally constrained peptides. This indicates that an interaction which involves these two residues may induce changes in the conformation of GnRH after it has bound to the receptor.
13
Nguyen, Kim Thoa Thi [Verfasser]. "Thyrotropin releasing hormone (TRH) selectively stimulates human hair follicle pigmentation / Kim Thoa Thi Nguyen". Lübeck : Zentrale Hochschulbibliothek Lübeck, 2017. http://d-nb.info/114120309X/34.
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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.
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Ngan, 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.
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Carter, Rebecca Ann. "Thyroid Status in Exercising Horses and Laminitic Ponies". Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/35454.
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The objective of these studies was to contribute to the understanding and assessment of thyroid function in horses. The first study evaluated methods of assessing thyroid function in horses, including validation of an enzyme immunoassay (EIA) for measuring equine thyroid hormones and development and assessment of a thyrotropin releasing hormone (TRH) response test. Our data indicated that EIA is an acceptable method for the measurement of total (T) and free (F) thyroxine (T4) and triiodothyronine (T3) in equine plasma. Its measurements are not equivalent to values obtained by radioimmunoassay (RIA), but they can be calibrated to predict corresponding RIA values. A protocol was developed for TRH response tests involving administration of 1 mg TRH intravenously, with blood sample collection immediately before, 2.5, 5.0, and 24 h after administration. Analysis of plasma TT4, FT4, TT3, and FT3 revealed that the magnitude of hormone response was best approximated by the area under the curve of hormone plotted against time and by the absolute change in thyroid hormone concentration. Baseline concentrations, peak concentrations, and percent of baseline values were not as well able to predict the magnitude of hormone response. The second study assessed the effects of exercise and feed composition on thyroid status. Thirteen mature Arabian geldings, adapted to either a high sugar and starch (SS) or high fat and fiber (FF) feed, underwent 15 wk of exercise training followed by a treadmill exercise test. The TRH response tests performed before training, after training, and the morning after the exercise test revealed that the exercise test decreased the TT4 and FT4 response, whereas feeding of high levels of sugars and starches increased the response of TT3 and FT3. During the first four weeks of training, increased TT4 and FT4 concentrations occurred simultaneously with increased nonesterified fatty acid concentrations, decreased triglyceride concentrations, and increased insulin sensitivity. The increase in TT4 and FT4 may have provided the cellular signaling necessary for increased lipolysis and insulin sensitivity. These metabolic changes facilitate the increases in lipid and carbohydrate metabolism that are needed to fulfill the additional energy requirements of regular exercise. The third study assessed thyroid status in ponies with different laminitic histories. Total T4, FT4, TT3, and FT3 were measured during March and May 2004 in 126 ponies that were categorized as either previously laminitic (PL; n = 54) or never laminitic (NL; n = 72) and evaluated for current laminitis in May (CL; n = 13). Decreased concentrations of TT4 and FT4 were found in PL ponies when compared to NL ponies in March (P = 0.018, 0.020) and May (P = 0.018, 0.001). However, TT4 and FT4 concentrations in CL ponies were not different than concentrations in NL ponies in May (P = 0.82, 0.72), and when retrospectively separated out in March, were not different than NL ponies (P = 0.90, 0.84). Therefore, basal thyroid hormone concentrations are not useful as a predictor or hormonal characteristic of pasture-associated laminitis. The decreased TT4 and FT4 in PL ponies may be an indication of a response or compensation to laminitis and may facilitate the metabolic changes necessary to cope with the disease.Master of Science
17
Chan, Koon-wing. "Molecular cloning and functional characterization of a goldfish growth hormone-releasing hormone receptor /". Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18539683.
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Hoo, 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.
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Papadopoulou, Nikoletta. "Investigation of the biological activity of corticotropin-releasing hormone receptors during pregnancy". Thesis, University of Warwick, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400089.
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Sedgley, Kathleen Ruth. "An investigation into the regulation and trafficking of gonadotrophin-releasing hormone receptors". Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431819.
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Hutchinson, 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.
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Gonadotropin-releasing hormone (GnRH), a central regulator of reproductive function in all vertebrates, exerts its effects via binding to the GnRH receptor (GnRHR) in the pituitary gonadotrophs. The GnRHR is a member of the G-protein coupled receptor (GPCR) superfarnily. A second form of the GnRHR (type II), other than the pituitary gonadotrope GnRHR (type I) has been proposed to exist and to play a role other than the classical endocrine role of the pituitary GnRHR. Elucidation of amino acid residues of the GnRHR that are crucial for ligand binding, activation of the receptor, and coupling to the G-protein, is important in understanding structure-function relationships towards the design of drugs for therapeutic intervention. Such information can often be deduced by a comparison between conserved and non-conserved amino acid residues of GnRHRs from different species. At the start of this project no non-mammalian or invertebrate, and only some of the eutherian mammalian type I GnRHRs had been cloned. The aim of this project was to clone novel GnRHRs, i.e. type I and type II GnRHRs from redbait and mole and type II mouse and human GnRHRs using polymerase chain reaction (PCR) strategies. PCR was performed with degenerate primers designed to human type I GnRHR to areas that are not conserved between GPCRs in general, but are conserved between mammalian GnRHRs.
22
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.
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Lee, 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.
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Fernandes, 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.
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Thesis (MSc)--University of Stellenbosch, 2007.ENGLISH 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.
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He, 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.
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Kee, Francis. "Aspartic acid scanning mutation analysis of a receptor isolated from goldfish specific to the growth hormone releasing hormone salmon-like peptide /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21827370.
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李景耀 i King-yiu Lee. "Molecular cloning and characterization of gonadotropin-releasing hormone receptors in the black seabream (Mylio macrocephalus)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224635.
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Fradinger, Erica Aileen. "Isolation and developmental expression of growth hormone-releasing hormone (GRF), pituitary adenylate cyclase-activating polypeptide (PACAP) and their receptors in the zebrafish, Danio rerio". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ62513.pdf.
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陳冠榮 i Koon-wing Chan. "Molecular cloning and functional characterization of a goldfish growthhormone-releasing hormone receptor". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31213923.
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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.
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The existence of an ultrashort feedback mechanism regulating GnRH secretion has been supported from in vivo and in vitro studies. However, the complex synaptic connections of GnRH neurons with other neural elements made it difficult to determine whether the regulation was mediated by direct actions on the GnRH neurons or through actions on other interneurons. The recent development of the GnRH-secreting neuronal cell line, GT1, provided a model system for the study of neural regulation of a pure population of GnRH neurons. The present studies utilized GT1 -7 cells to investigate whether GnRH (at the level of the nerve terminal) influences the control of its own release. Preliminary studies determined the presence of GnRH mRNA in GT1-7 cells and established a cell culture system for the analysis of secretagogue-induced GnRH release. In this system GnRH release was shown to be spontaneous and was enhanced by the addition of K⁺, L-GLU, forskolin and PMA. Furthermore, K⁺- and forskolin-induced GnRH release was dependent on extracellular Ca²⁺. For the analysis of an ultrashort feedback mechanism, GT1-7 cells were cultured in 6-well plates to near confluence and then incubated in serum-free medium in the presence (1 nM- 1 μM) or absence of GnRH antagonist, Ant 27. Basal, K⁺-and forskolin-induced secretion of GnRH was monitored with antiserum 1076 which does not cross-react with Ant 27 at> 1 μM. Ant 27 treatment increased basal, K⁺- and forskolin-stimulated GnRH release in a dose-dependent manner. Total content was unaffected by 18 h treatment of GT1-7 cells with Ant 27. This suggests that the effects of Ant 27 are at the level of release and not biosynthesis. The presence of GnRH binding sites in the cells was demonstrated with ¹²⁵I-GnRH analog. These findings support the concept that GnRH, acting via autoreceptors, negatively controls its own release.
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紀思思 i Francis Kee. "Aspartic acid scanning mutation analysis of a receptor isolated from goldfish specific to the growth hormone releasing hormone salmon-likepeptide". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31222766.
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Sadie, 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.
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Thesis (PhD (Biochemistry))--University of Stellenbosch, 2006.Gonadotropin-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.
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Lee, ChangWoo. "CIS- AND TRANS-ACTIVATION OF HORMONE RECEPTORS: THE LH RECEPTOR". Lexington, Ky. : [University of Kentucky Libraries], 2003. http://lib.uky.edu/ETD/ukybiol2003d00082/changwoo.pdf.
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Thesis (Ph. D.)--University of Kentucky, 2003.Title from document title page. Document formatted into pages; contains xix, 74p. : ill. Includes abstract. Includes bibliographical references (p. 62-72).
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Faurholm, Bjarne. "Gene structure, transcripts and transcriptional regulation of primate type II gonadotropin-releasing hormone receptors". Doctoral thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/3127.
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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.
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Van, 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.
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Dissertation (PhD)--University of Stellenbosch, 2006.ENGLISH 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.
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Tam, Sau-ping. "Gene expression of hypothalamic somatostatin, growth hormone releasing factor, and their pituitary receptors in hypothyroidism /". Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17538865.
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Shortridge, Emily. "The Cryptic Peptides, Prepro-Thyrotropin Releasing Hormone 186-199 and 194-199, Suppress Anterior Pituitary Prolactin Secretion in vivo and in vitro". Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/221632.
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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.Prepro-thyrotropin releasing hormone (ppTRH)-176-199 is one of several peptide fragments cleaved during TRH synthesis and has been implicated as a regulator of neuroendocrine function. ppTRH 176-199 has been shown to acutely inhibit the stress-induced rise in ACTH, corticosterone (CORT), and prolactin (PRL) in the rat. The receptor for ppTRH 176-199 currently remains unknown. In this study we sought to characterize the active domain of ppTRH 176-199 and, using in vivo and in vitro approaches, determine its role in regulating anterior pituitary secretion of PRL. The 186-199, 194-199, and 186-191 amino acid fragments of ppTRH were administered I.P. to adult male Sprague-Dawley rats 15 min. prior to a 20 min restraint stress to determine the peptide’s active moiety in regulating prolactin secretion. Animals were euthanized and plasma was saved for assay of circulating PRL using enzyme immunoassay (EIA). ppTRH 186-199 significantly attenuated the stress-induced rise in prolactin in male rats in a dose-responsive fashion. This effect was mimicked by ppTRH 194-199 but not by ppTRH 186-191. At the highest dose (10 mg/kg BW), ppTRH 194-199 also reduced the stress-induced rise in plasma CORT. Additionally, in vitro studies were performed using the rat growth hormone (GH)/PRL –secreting MMQ cell line. MMQ cells were treated with ppTRH 186-199 and media was assayed for PRL levels. Cells were harvested and examined for changes in PRL mRNA. Within 30 minutes following treatment of estradiol-stimulated MMQ cells with ppTRH 186-199 there was a decrease in media levels of PRL compared to vehicle. Furthermore, in MMQ cells that were primed with 10nM estradiol for 48 hours there was an increase in media PRL levels, which was reduced following ppTRH 186-199 treatment. After 4 hrs of treatment, the inhibitory effect of ppTRH 186-199 on PRL secretion from MMQ cells was only seen on estradiol-stimulated cells. There were no effects of ppTRH 186-199 when examined after 24 hrs of treatment. There were no effects of ppTRH 186-199 or 194-199 of PRL mRNA levels. These data suggest that the carboxy terminal fragment of preproTRH 178-199 contains all the activity of this ppTRH cryptic peptide for regulation of PRL and corticosterone secretion. This suggests a potential moiety responsible for interaction with the peptide’s receptor. The inhibitory effect of ppTRH 186-199 and 194-199 on media PRL levels and not on mRNA synthesis implicates it as an effector of hormone secretion rather than protein synthesis. The short-lived duration of its effects supports a role as 6 an acute effector of the PRL system. The target receptor of the ppTRH 178-199 fragment remains uncertain. However the use of ppTRH 194-199 as a peptide bait may prove useful in identifying the receptor.
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Romanowski, Christoph. "The involvement of central corticotropin-releasing hormone and its receptors in sleep-wake regulation of mice". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-118519.
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Yamamoto, Akane. "Response of preterm infants with transient hypothyroxinaemia of prematurity to the thyrotropin-releasing hormone stimulation test is characterized by a delayed decrease in thyroid-stimulating hormone after the peak". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263539.
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Bertacchini, Eleonora. "Molecular study of stress system in the European sea bass (Dicentrarchus labrax): cloning of different components and effects of essential oil of Lippia alba during stress situation". Master's thesis, Alma Mater Studiorum - Università di Bologna, 2018.
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European sea bass (Dicentrarchus labrax) is one of the most important species in the Mediterranean aquaculture. In this context, fish are subjected to practices that activate the stress system and can adversely affect their health and welfare. To minimise the effects of stress on fish, investigators have begun to examine the use of natural products with anaesthetic properties that are more effective, safer and less expensive than the currently available synthetic drugs. The aim of the present study was to assess the effectiveness of the essential oil of Lippia alba (EOLA) to mitigate the stress response in D. labrax individuals disturbed by persecution. For this purpose, sea basses were subjected to 3 and 6 hours of stress procedure and sedated with two different concentrations of the EOLA, 25 and 50 μL L-1. Partial cDNA sequences of crhbp and trh genes were cloned and their mRNA expression, together with that of crh, pomc, star, nr3c1 and nr3c2, all stress-related genes of the hypothalamus-pituitary-interrenal axis, were analysed in different tissues. Results elucidated that the most conspicuous variations in gene expression were found out for crh at 6 hours, which pattern was inversely proportional to cortisol levels. This may indicate the existence of a negative feedback mechanism exerted by cortisol. Expression of mineralocorticoid and glucocorticoid receptors (nr3c1 and nr3c2) showed a trend that diverged in relation to the belonging tissue, but in hypothalamus it mirrored the variation of crh, highlighting again a role of cortisol in regulating gene expression during the stress response. Furthermore, an appreciable increment in trh mRNA occurred in every treatment after 3 hours, suggesting that this hormone can be involved in the stress response. The best concentration of EOLA in order to reduce stress is represented by 25 μL L-1. On the contrary, at 50 μL L-1, the oil can be itself a stressor and after 6 hours it loses its effectiveness and it degrades.
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Wang, Ying, i 王莹. "Molecular and functional characterization of the prolactin receptor, prolactin-releasing peptide receptor, and growth hormone-releasinghormone receptor genes in chicken". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39556864.
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Eymin, Cécile. "Étude des récepteurs de la sérotonine et de la thyrotropin-releasing hormone dans l'hippocampe humain normal et pathologique : mort subite du nourrisson et suicide". Lyon 1, 1993. http://www.theses.fr/1993LYO1T108.
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Leung, Kin-yue. "Involvement of NF-kB subunit p65 and retinoic acid receptors RARæ and RXRæ in the transcriptional regulation of the human GnRH II gene". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36367035.
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Karteris, Emmanouil. "Expression and signal transduction characteristics of the corticotropin-releasing hormone (CRH) receptors in human placenta and fetal membranes". Thesis, University of Warwick, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364678.
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Troskie, Brigitte Elise. "Cloning and characterisation of gonadotropin-releasing hormone receptors from species in non-mammalian vertebrate classes : amphibia and osteichthyes". Doctoral thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26916.
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Two or more forms of gonadotropin-releasing hormone (GnRH) have been isolated from most vertebrate species. In most species, GnRH variants have been shown to occur in distinct areas of the peripheral and central nervous systems, the gonads and other peripheral organs. Although GnRH is a primary regulator of gonadotropin secretion, it has been shown to have additional roles such as the regulation of growth hormone secretion in goldfish and the inhibition of a potassium current (M-current) in amphibian sympathetic ganglia. This raises the possibility of the occurrence of multiple GnRH receptor subtypes. This thesis describes the cloning and characterisation of GnRH receptor subtypes from two nonmammalian vertebrates, the Amphibian, Xenopus laevis and the Osteichthyes, Carassius auratus (goldfish). Using degenerate primers designed to the mammalian GnRH receptors two putative receptor subtypes were identified from both X. laevis (X/a.1 and X/b.1) and goldfish (GfA and GfB) genomic DNA. The full-length cDNA for X/a.1, was cloned from pituitary cDNA. When transiently expressed in COS-1 cells, this clone showed a GnRH-dependent stimulation of inositol phosphates. No full-length clone for X/b.1 could be isolated using cDNA from several different tissues. A partially processed transcript was, however, amplified from sympathetic ganglia cDNA. These ganglia showed specific binding to a chicken GnRH II (cGnRH II) agonist and cGnRH II immunoreactivity was also detected in extracts from the ganglia. The expression, function and pharmacology of clone X/b.1, thus remains unknown, but the presence of cGnRH II-specific binding sites on membranes from the sympathetic ganglia with distinctly different pharmacology, implies the presence of a second GnRH receptor subtype in these neurons. Full-length cDNA clones of GfA and GfB were amplified from goldfish pituitary and brain cDNA respectively. These receptors had a 71% amino acid identity to each other and a 43% amino acid identity to the human GnRH receptor. The pharmacology of these two GnRH receptor subtypes was investigated by transient expression in COS-1 cells. The GfA and GfB receptors had different pharmacologies as demonstrated by their selectivities for GnRH analogues. In situ hybridisation revealed a distinct expression pattern of the goldfish GnRH receptor subtypes in the brain, gonads and liver (Dr R. Peter, University of Alberta). The full-length receptors cloned from the pituitaries and brain of X. /aevis and the goldfish have a low homology to the cloned mammalian GnRH receptors and have several different features, such as the presence of an intracellular carboxy-terminal tail. This thesis, describing the primary structure and characterisation of ligand selectivity of non-mammalian GnRH receptors, provides some useful foundations for future work towards understanding ligand recognition in the GnRH receptor. The description of multiple receptor subtypes in the goldfish and possibly in X. laevis also provides valuable information into alternative roles of GnRH and its receptor, which we are only beginning to understand.
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Leung, Kin-yue, i 梁建裕. "Involvement of NF-kB subunit p65 and retinoic acid receptors RARæ and RXRæ in the transcriptional regulation of the human GnRH II gene". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36367035.
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Styger, Gustav. "The role of steroidogenic factor-1 (SF-1) in transcriptional regulation of the gonadotropin-releasing hormone (GnRH) receptor gene". Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52572.
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Thesis (MSc)--Stellenbosch University, 2001.ENGLISH ABSTRACT: The GnRH receptor is a G-protein-coupled receptor in pituitary gonadotrope cells. Binding of its ligand, GnRH, results in synthesis and release of gonadotropin hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH). Steroidogenic factor 1 (SF-1), a transcription factor, binds to specific sites in the promoter region of gonadotropin genes, and thus regulates transcription of these genes. The promoter region of the GnRHreceptor gene contains two SF-1-like binding sites, one at -14 to -8 (site 1) and another at -247 to -239 (site 2), relative to the methionine start codon. The role played by these two SF-1-like sites in basal transcription of the mouse GnRH receptor (mGnRH-R) gene in a pituitary precursor gonadotrope cell line, aT3 cells, was the first area of investigation during this study. Luciferase reporter constructs containing 580 bp of mGnRH-R gene promoter were prepared, where SF-1-like sites were either wildtype or mutated. Four such constructs were made, i.e. wildtype (LG), site 1 mutant (LGM1), site 2 mutant (LGM2) and mutated site 1 plus site 2 (LGM1/2). These constructs were transfected into aT3 cells to determine the effect of mutations of sites 1 and/or 2 on the basal expression of the mGnRH-R gene. Mutation of either site 1 or site 2 had no effect on basal expression of the mGnRH-R gene. It was found that only upon simultaneous mutation of both sites 1 and 2, a 50% reduction in basal transcription took place. The implications of this is that SF-1 protein seems to only require one intact DNA-binding site, to mediate basal transcription of the mGnRH-R gene, suggesting that these two sites lie in close proximity during basal transcription. The effect of the protein kinase A (PKA) pathway on the endogenous mGnRH-R gene was also investigated by incubating non- , transfected aT3 cells with the PKA activators, forskolin and 8-Br-cAMP. Similar incubations were also performed on the wild type and mutated site 1 constructs transfected into pituitary gonadotrope aT3 cells. It was found that forskolin and 8-Br-cAMP were able to increase endogenous mGnRH-R mRNA levels in a concentration-dependent fashion, showing that endogenous GnRH receptor gene expression is stimulated via a protein kinase A pathway. Similar results were obtained with the wildtype promoter construct, showing that the protein kinase A pathway stimulates transcription of the promoter. This effect was only seen with wild type and not with the mutated site 1. These results are consistent with a role for a SF-1-like transcription factor in mediating the protein kinase A effect via binding to the site 1 at position -14 in the GnRH receptor gene. A separate investigation was performed to determine whether 25-hydroxycholesterol (25-0HC) is a ligand for SF-1, by incubating aT3 cells transfected with the various constructs with 25-0HC. Results show a dose-dependant response, with an increase in gene expression at 1 μM and a decrease at higher concentrations, for both mutant and wild type constructs. This suggests that, if SF-1 is indeed the protein binding to sites 1 and 2, then 25-0HC is not a ligand for SF-1 protein in aT3 cells and that the effect of 25-0HC on the mGnRH-R gene is not mediated via site 1. The results indicate that these decreases of expression at the higher concentrations may be due to cytotoxic effects. Towards the end of the study the laboratory obtained a luminoskan instrument with automatic dispensing features. Optimisation studies on the luciferase and β-Gal assays were performed on the luminoskan in a bid to decrease experimental error. It was found that automation of these assays resulted in a decrease in experimental error, showing that future researchers could benefit substantially from these optimisation studies.
AFRIKAANSE OPSOMMING: Die GnRH reseptor is 'n G proteïen-gekoppelde reseptor in pituitêre gonadotroopselle. Binding van die ligand, GnRH, lei tot die sintese en vrystelling van die gonadotropien hormone, luteïniserende hormoon (LH) en follikel stimulerende hormoon (FSH). Steroidogeniese faktor-t (SF-1) is 'n transkripsie faktor wat aan spesifieke areas in die promotergebied van die gonadotropien hormone bind, en dus transkripsie van hierdie gene reguleer. Die promotergebied van die GnRH reseptor geen bevat twee SF-1 bindings areas, een by -14 to -8 (area 1) asook by -247 to -239 (area 2), relatief to die metionien beginkodon. Die rol wat hierdie twee SF-1 areas speel in basale transkripsie van die muis GnRH reseptor (mGnRH-R) geen in 'n pituïtêre voorloper gonadotroop sellyn, aT3 selle, was die eerste gebied van ondersoek gedurende hierdie studie. Plasmiede bestaande uit die 580 basispaar mGnRH-R promoter verbind aan 'n lusiferase geen is vervaardig, waar SF-1-soortige areas enersyds onveranderd gelaat is, of gemuteer is. Vier sulke plasmiede is vervaardig, nl. onveranderd (LG), area 1 mutant (LGM1), area 2 mutant (LGM2) en gemuteerde area 1 plus area 2 (LGM1/2). Hierdie plasmiede is gebruik om aT3 selle te transfekteer om die effek van mutasies van areas 1 en/of 2 op die basale ekspressie van die mGnRH-R geen te ondersoek. Daar is gevind dat mutasies van areas 1 of 2 geen effek op basale ekspressie op die bogenoemde geen gehad het nie. Slegs tydens gelyktydige mutasie van areas 1 en 2 het 'n 50% vermindering in basale transkripsie plaasgevind. Die implikasies hiervan is dat die SF-1 proteïen blykbaar slegs een volledige DNA-bindingsarea benodig om basale transkripsie van die mGnRH-R geen te reguleer. Dit wil dus voorkom of hierdie twee areas baie na aan mekaar geposisioneer is tydens basale transkripsie. Die effek van die proteïen kinase A (PKA) roete op die natuurlike mGnRH-R geen is ook ondersoek tydens inkubasie van nie-getransfekteerde aT3 selle met die PKA akiveerders, forskolin en 8-Br-cAMP. Soortgelyke inkubasie is ook gedoen op die onveranderde en gemuteerde area 1 plasmiede wat in aT3 selle getransfekteer is. Daar is gevind dat forskolin en 8-Br-cAMP daarin geslaag het om die natuurlike mGnRH-R geen mRNA vlakke op 'n konsentrasie-afhanklike wyse te vermeerder. Hierdie resultaat dui daarop aan dat die natuurlike mGnRH-R geen se ekspressie gestimuleer kan word via 'n proteïen kinase A roete. Soortgelyke resultate is verkry met die onveranderde promoter plasmied en dit wys ook daarop dat proteïen kinase A transkripsie deur die promoter kan stimuleer. Hierdie effek was slegs aanwesig met die onveranderde en nie met die gemuteerde area 1 plasmied nie. Die resultate stem ooreen met 'n rol vir SF-1 transkripsie faktor in die regulering van proteren kinase A effek deur middel van binding aan die area 1 by posisie -14 in die GnRH-R geen. 'n Afsonderlike ondersoek is gedoen om vas te stel of 25-hidroksiecholesterol (25-0HC) 'n ligand vir SF-1 is deur getransfekteerde aT3 selle met 25-0HC te inkubeer. Resultate toon 'n dosis-afhanklike respons met 'n verhoging in geen ekspressie by 1 μM en 'n verlaging met hoër konsentrasies vir beide onveranderde en gemuteerde plasmiede. Dit impliseer dat, indien SF-1 wel die faktor is wat aan areas 1 en 2 bind, 25-0HC nie die ligand vir SF-1 proteren in aT3 selle is nie en dat die effek van 25-0HC op die mGnRH-R geen nie gereguleer word via area 1 nie. Die verlaging in ekspressie gevind by die hoër konsentrasies is dalk die gevolg van sitotoksiese effekte. Teen die einde van die studie het die laboratorium luminoskan toerusting met outomatiese pipettering verkry. Optimiseringstudies van die lusifirase en β-Galtoetse is met die luminoskan gedoen in 'n poging om eksperimentele foute te minimaliseer. Daar is gevind dat outomatisering van hierdie toetse wel gelei het tot 'n verlaging in eksperimentele foute. Toekomstige navorsers kan dus grootliks voordeel trek uit hierdie optimiseringstudies.
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Morley, Michelle Gaye. "Cloning and characterisation of gonadotropin-releasing hormone (GnRH) receptors in the cichlid (Haplochromis burtoni) and the zebrafish (Danio rerio)". Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/6949.
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Bibliography: leaves 75-89.The identification of multiple forms of gonadotropin-releasing hormone (GnRH) in a single species is becoming a common occurrence. The highly conserved chicken GnRH II is present along with one or two other GnRHs, composing a combination unique to particular species. This multifunctional peptide is widely distributed through the central nervous system and peripheral tissues. Also, endogenous GnRHs demonstrate distinct patterns of spatial expression within the brain, suggesting they may have separate functions. In addition to being the primary regulator of gonadotropin secretion in vertebrates, GnRH is also involved in the release of GH and prolactin and may fulfil a possible neuromodulatory role. GnRHs exert their actions through the stimulation of distinct GnRH receptors on pituitary gonadotrophs. The presence of multiple GnRH receptor subtypes has been demonstrated in several species and is likely to be a common characteristic of most vertebrates. This thesis describes the cloning and characterisation of GnRH receptors in two species of teleost fish, Haplochromis burtoni (cichlid) and Dania rerio (zebrafish). A type I GnRH receptor has previously been shown to exist in the cichlid. In the present study degenerate primers designed to extracellular loop three of the mammalian GnRH receptors were used to identify a second putative receptor subtype from cichlid (Haplochramis burtoni) genomic DNA. Furthermore, a near full-length cDNA, encompassing transmembrane domain 1 through to transmembrane domain 7 of the GnRH receptor, was cloned from cichlid RNA by reverse transcriptase PCR. This region of the receptor shares approximately 80% amino acid homology with corresponding regions of type III GnRH receptors previously identified in species of perciform fish. Partial sequences of a type IA and a type lB GnRH receptor have previously been identified in the zebrafish. Two sets of degenerate primers were used to elucidate the possible existence of a third receptor in the zebrafish using both genomic DNA and RNA. However, this strategy failed to result in the amplification of novel receptor subtypes in the zebrafish. Controversy surrounds the developmental origins of GnRH neurons and their temporal expression in relation to GnRH receptors. The zebrafish is a model organism, widely used for the study of reporter gene expression during development. Hence an attempt was made to isolate the zebrafish GnRH receptor genes using a genomic DNA library and identify the promoter regions for use as reporter genes in the study of GnRH and GnRH receptor expression during development. Southern blot analysis revealed six genomic clones with sequences homologous to zebrafish GnRH receptor cDNA. Comparison with genomic and cDNA sequences of other GnRH receptors revealed that those regions of the genomic clones that were sequenced only encoded exons 2 and 3. The presence of large introns in the GnRH receptor gene made it difficult to identify genomic clones containing the entire gene and the promoter region. The cloning of part of the zebrafish GnRH receptor genes will make their complete characterisation somewhat less problematic since an idea of their basic intron/exon structure has been obtained. Exons 2 and 3 of the zebrafish type IA and type IB GnRH receptor genes show a high degree of conservation when compared to the same regions of the goldfish type IA and type IB GnRH receptor cDNAs, demonstrating approximately 90% homology in both cases. In this study sequence information was obtained for the regions between transmembrane domains 4 and 7, and 3 and 7 of the zebrafish type IA and type IB GnRH receptor genes, respectively, and was subsequently used clone zebrafish GnRH receptor full-length cDNAs. This study describes the discovery of a type III GnRH receptor in the cichlid but suggests its presence may be restricted to only certain orders of teleost since a type III receptor was not identified in the zebrafish on this occasion. The information acquired from this study may help to reveal patterns, which relate the presence of particular GnRHs and GnRH receptors in single species to specific reproductive requirements.
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Trouslard, Jérôme. "Etude electrophysiologique du couplage excitation-secretion des cellules endocrines du lobe intermediaire de l'hypophyse : mise en evidence d'un effet excitateur medie par la thyrotropin-releasing hormone". Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR13072.
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Nous avons developpe une culture primaire de cellules endocrines du lobe intermediaire de l'hypophyse (cellules melanotropes) de porc sur lesquelles nous avons applique la technique electrophysiologique du patch-clamp. Nous avons caracterise un courant sodique tetrodotoxine sensible, trois courants calciques (t, l, n), un courant potassique retarde et un courant potassique transitoire. Ces courants s'integrent sous la forme de deux modes d'activite spontanee: une activite de potentiels d'action rapides de nature sodique et une activite de bouffees de potentiels d'action sodico-calciques. L'originalite de notre travail consista a mettre en evidence l'effet excitateur de la thyrotropin-releasing hormone (trh) sur le couplage stimulation-secretion de la cellule melanotrope de ce mammifere. La trh augmente la frequence de decharge de potentiels d'action, la secretion et la synthese hormonales. Au plan biochimique, nous confirmons le couplage du recepteur trh a une phospholipase c