Relevant bibliographies by topics / Gonadotropin releasing hormone

Academic literature on the topic 'Gonadotropin releasing hormone'

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Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Gonadotropin releasing hormone"

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Schwartz, Neena B. "The 1994 Stevenson Award Lecture. Follicle-stimulating hormone and luteinizing hormone: a tale of two gonadotropins." Canadian Journal of Physiology and Pharmacology 73, no. 6 (June 1, 1995): 675–84. http://dx.doi.org/10.1139/y95-087.

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Although most gonadotropes synthesize both luteinizing hormone and follicle-stimulating hormone, the transcription, content, and secretion rates of the two gonadotropins can be separated. The signals external to the gonadotropic cells that appear to be important in the differential regulation are gonadotropin-releasing hormone pulse frequency (high pulse frequency favors luteinizing hormone), steroid feedback (works on both but induces a more powerful negative feedback on luteinizing hormone), and gonadal peptide feedback (activin increases follicle-stimulating hormone; inhibin and follistatin decrease it). We know very little about the pathways within the gonadotropes that favor one gonadotropin rather than another. It is expected that the cloning of the genes for both gonadotropins and the use of specific cell lines and transfections will lead to elucidation of these pathways.Key words: luteinizing hormone, follicle-stimulating hormone, gonadotropin-releasing hormone, inhibin, anterior pituitary, gonads.
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Podhorec, P., and J. Kouril. "Induction of final oocyte maturation in Cyprinidae fish by hypothalamic factors: a review." Veterinární Medicína 54, No. 3 (April 8, 2009): 97–110. http://dx.doi.org/10.17221/50/2009-vetmed.

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Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.
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Braden, Tim D., and P. Michael Conn. "The 1990 James A. F. Stevenson Memorial Lecture. Gonadotropin-releasing hormone and its actions." Canadian Journal of Physiology and Pharmacology 69, no. 4 (April 1, 1991): 445–58. http://dx.doi.org/10.1139/y91-067.

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Gonadotropin-releasing hormone (GnRH) stimulates the release and biosynthesis of gonadotropins, luteinizing hormone, and follicle-stimulating hormone from the pituitary gland. Additionally, GnRH regulates the number of its own receptors on pituitary gonadotropes causing both up- and down-regulation of receptors as well as biosynthesis of GnRH receptors. After exposure to GnRH, gonadotropes become desensitized to further stimulation by GnRH. The mechanisms through which these actions of GnRH are mediated appear to differ. Effects dependent upon extracellular calcium include gonadotropin biosynthesis and release as well as up-regulation of GnRH receptors. Additional actions of GnRH, such as down-regulation of receptors, biosynthesis of receptors, and desensitization, appear to be independent of extracellular calcium. Subsequent studies have ascribed roles for calmodulin and protein kinase C in mediating specific effects of GnRH.Key words: pituitary, gonadotropin-releasing hormone, receptor, protein kinase C, calmodulin.
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&NA;. "Gonadotropin releasing hormone." Reactions Weekly &NA;, no. 800 (May 2000): 8. http://dx.doi.org/10.2165/00128415-200008000-00021.

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Chow, Billy K. C. "Gonadotropin-releasing hormone." FEBS Journal 275, no. 22 (October 6, 2008): 5457. http://dx.doi.org/10.1111/j.1742-4658.2008.06675.x.

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Wiwanitkit, Viroj. "Model of gonadotropin-releasing hormone and gonadotropin-releasing hormone complex." Sexuality and Disability 24, no. 3 (September 2006): 175–78. http://dx.doi.org/10.1007/s11195-006-9018-4.

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Burger, L. L., D. J. Haisenleder, A. C. Dalkin, and J. C. Marshall. "Regulation of gonadotropin subunit gene transcription." Journal of Molecular Endocrinology 33, no. 3 (December 2004): 559–84. http://dx.doi.org/10.1677/jme.1.01600.

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Reproductive function in mammals is regulated by the pituitary gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH and FSH are secreted by the gonadotrope cell and act on the gonad in a sequential and synergistic manner to initiate sexual maturation and maintain cyclic reproductive function. The synthesis and secretion of LH and FSH are regulated mainly by the pulsatile release of the hypothalamic decapeptide hormone gonadotropin-releasing hormone (GnRH). The control of differential LH and FSH synthesis and secretion is complex and involves the interplay between the gonads, hypothalamus and pituitary. In this review, the transcriptional regulation of the gonadotropin subunit genes is discussed in a physiologic setting, and we aimed to examine the mechanisms that drive those changes.
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TRUDEAU, V., A. PHARAZYN, F. X. AHERNE, and E. BELTRANENA. "NALOXONE ELEVATES PLASMA FOLLICLE STIMULATING HORMONE BUT NOT LUTEINIZING HORMONE LEVELS IN THE IMMATURE MALE PIG." Canadian Journal of Animal Science 69, no. 4 (December 1, 1989): 1095–98. http://dx.doi.org/10.4141/cjas89-126.

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The effects of intraperitoneal injection of gonadotropin-releasing hormone (GnRH) alone, naloxone (NAL) alone, or in combination on plasma levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) was studied in 4- to 5-wk-old male pigs. GnRH (1 μg kg−1) effectively stimulated (P < 0.05) secretion of both gonadotropins whereas NAL (1 and 10 mg kg−1) stimulated only FSH secretion (P < 0.05). There was no interaction between GnRH and NAL on gonadotropin release. These results suggest that endogenous opiates are involved in the regulation of FSH secretion but not LH secretion in the immature male pig. Key words: Follicle-stimulating hormone, luteinizing hormone, naloxone, gonadotropin-releasing hormone, male pig
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ALI, A., A. ELTOBGY, H. ELAZIZ, S. ELSHAYEB, M. ELDIN, and A. ELAZEEMSARHAN. "Gonadotropin-releasing hormone mRNA, gonadotropin-releasing hormone peptide, and variants of gonadotropin-releasing hormone receptor in human placenta." Obstetrics & Gynecology 93, no. 4 (April 1999): S5. http://dx.doi.org/10.1016/s0029-7844(99)90007-8.

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Sasaki, Kirsten, and Errol R. Norwitz. "Gonadotropin-releasing hormone/gonadotropin-releasing hormone receptor signaling in the placenta." Current Opinion in Endocrinology & Diabetes and Obesity 18, no. 6 (December 2011): 401–8. http://dx.doi.org/10.1097/med.0b013e32834cd3b0.

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Dissertations / Theses on the topic "Gonadotropin releasing hormone"

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Gardner, Samantha. "Gonadotropin-releasing hormone targets Wnt signalling." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29112.

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This thesis describes a potential mechanism by which GnRH promotes the nuclear accumulation of β-catenin, activation of TCF-dependent transcription and up-regulation of Wnt target genes, c-Jun, Fra-1, Cyclin D1 and c-Mye. GnRH-induced nuclear accumulation of β-catenin and activation of β-catenin/TCF-dependent transcription was found to be dependent on a pathway utilising Gq-Phospholipase C (PLC)-Diacylglycerol (DAG)/Protein kinase C (PKC), and was found to be specifically dependent on the PKC δ isoform. GnRH was found to mediate the inactivation of Glycogen Synthase Kinase-3 (GSK-3), a protein serine/threonine kinase that regulates β-catenin degradation within the canonical Wnt signalling pathway. These results were observed in HEK293/GnRH receptor expressing cells and have been recapitulated in LβT2 and αT3-1 mouse gonadotrope cells, and then extended to various peripheral cell lines, sub-cultured prostate cells and whole prostate organ cultures. A potential mechanism of non-canonical Wnt/Ca2+ pathway activation by GnRH is described. GnRH was found to activate NFAT, a potential effecter of the non-canonical Wnt/Ca2+ pathway. GnRH-induced NFAT activation was found to be dependent on important mediators of the non-classical Wnt/Ca2+ pathway, including Gq, Ca2+, Calcineurin and PKC δ.  Intriguingly, by expression of a dominant negative TCF construct, GnRH-induced NFAT activation was found to be TCF-dependent, thereby implicating TCF in targeting both Wnt/β-catenin and Wnt/Ca2+ signalling. This novel finding suggests that a TCF-NFAT interaction may exist that functions either, to inhibit β-catenin/TCF-dependent transcription through competition for nuclear TCF, or to synergistically regulate TCF- and NFAT-target gene expression.
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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.
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李繼仁 and 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.

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Lee, 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.

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顔秀慧 and 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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Cronin, 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.

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The studies described in this thesis investigated the hypothesis that the development of GnRH neurite outgrowth is promoted by BDNF. The objectives were to establish whether BDNF and its receptor TrkB were expressed in regions associated with developing GnRH neurons, and then to ascertain whether BDNF elicited neurotrophic effects in GnRH neurons. In situ hybridisation revealed that during development from E12.5 to adult, BDNF mRNA was found throughout the hypothalamus, from the POA to the medial basal hypothalamus. TrkB mRNA (which encodes the receptor for BDNF) was found in the region of the olfactory tracts and bulbs at E14.5-16.5, and throughout the brain from E16.5 to adulthood. Furthermore, the majority of cultured embryonic GnRH cells were immunoreactive for TrkB. These primary cell cultures were used to investigate the actions of BDNF on GnRH neurite outgrowth. Treatment with BDNF for 39 hours induced a significant increase in the length of neurites, but had no discernible affect on branching. Subsequent investigations into the signalling pathway by which BDNF may exert this response revealed induction of phospho-Ca2+/cAMP response element-binding protein (pCREB) in GnRH and non-GnRH cells following an acute BDNF treatment. BDNF is known to induce phosphorylation of CREB in other neuronal types via the Ras-microtubule associated protein kinase/extracellular-regulated kinase (Ras-MAPK/ERK) pathway which also results in neurite outgrowth, so the response to BDNF of ERK, an upstream MAP kinase of CREB, was also tested in GnRH cells. It was discovered that pCREB was induced in GnRH cells following treatment with BDNF, but this was not associated with induction of pERK, though BDNF treatment did stimulate pERK in neighbouring non-GnRH cells. In summary, GnRH cells possess the receptor for BDNF, TrkB, and that during their development, the neurites they elaborate course through BDNF-rich areas of the brain.
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Kirkpatrick, 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.

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Endocrine regulation of expression of GnRH receptors is an important step in the control of reproduction. During the early follicular phase of the estrous cycle in the ewe, GnRH receptor expression increases in preparation for the preovulatory surge of LH. The studies described herein were designed to further elucidate the hormonal interactions controlling GnRH receptor expression. In long-term ovariectomized ewes, neither removal of progesterone, nor the presence of estradiol affected the expression of GnRH receptors. However, in ewes ovariectomized during the luteal phase of the estrous cycle and immediately implanted with progesterone and estradiol for 48 hours, low levels of estradiol for 24 hours were required to increase GnRH receptor mRNA following the removal of progesterone. In ovariectomized ewes following hypothalamic-pituitary disconnection, low levels of estradiol and pulsatile GnRH were required to increase GnRH receptor expression within 24 hours of treatment initiation. These results suggest an interaction between estradiol and GnRH is involved in increasing GnRH receptor expression during the periovulatory period. How progesterone, estradiol and, GnRH interact to increase GnRH receptors is unknown, but a possible candidate involved in mediating these interactions may be the cell specific transcription factor, steroidogenic factor-1 (SF-1). SF-1 mRNA increased within 24 hours of treatment of ewes with prostaglandin F₂(α) compared to ewes in the luteal phase of the estrous cycle. This suggests that progesterone may have an inhibitory effect on SF-1 mRNA. SF-1 mRNA was similar between ovariectomized ewes and ovariectomized ewes following hypothalamic-pituitary disconnection treated with estradiol and GnRH. Treatment with estradiol or GnRH alone did not increase SF-1 mRNA. The results of these experiments suggest that progesterone removal as well as the presence of estradiol and GnRH are required to increase GnRH receptor expression during the early follicular phase in the ewe. Further, the transcription factor, SF-1 may be involved in mediating the effects of these hormones on GnRH receptor expression.
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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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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.
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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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Books on the topic "Gonadotropin releasing hormone"

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L, Barbieri Robert, and Friedman Andrew J, eds. Gonadotropin releasing hormone analogs: Applications in gynecology. New York: Elsevier, 1991.

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Jan, Horský. Gonadotropin-releasing hormone and ovarian function. Prague: Avicenum, Czechoslovak Medical Press, 1986.

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1958-, Parhar Ishwar S., ed. Gonadotropin-releasing hormone: Molecules and receptors. Amsterdam: Elsevier, 2002.

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Goodman, Stephanie Robin. Effects of gonadotrophin releasing hormone on growth hormone release in the rat. [New Haven, Conn: s.n.], 1993.

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World, Congress on Fertility and Sterility (15th 1995 Bologna Italy). Treatment with GnRH analogs: Controversies and perspectives : the proceedings of a satellite symposium of the 15th World Congress on Fertility and Sterility held in Bologna, Italy, 15-16 September 1995. New York: Parthenon Pub. Group, 1996.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Gore, Andrea C. GnRH, the master molecule of reproduction. Boston: Kluwer Academic Publishers, 2002.

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Nyean, Lee Chin, ed. Using gonadotropin-releasing hormone (GnRH) to improve dairy cattle conception rates in the tropics. [Honolulu]: HITAHR, College of Tropical Agriculture and Human Resources, University of Hawaii, 1989.

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Organon Round Table Conference (3rd 1992 Paris, France). GnRH, GnRH analogs, gonadotropins, and gonadal peptides: The proceedings of the third Organon Round Table Conference, Paris, 1992. London: Parthenon Pub. Group, 1993.

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Book chapters on the topic "Gonadotropin releasing hormone"

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Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow, et al. "Gonadotropin-Releasing Hormone." In Encyclopedia of Psychopharmacology, 561. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1886.

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Naor, Zvi, and Rony Seger. "Gonadotropin-Releasing Hormone." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2477-2.

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Naor, Zvi, and Rony Seger. "Gonadotropin-Releasing Hormone." In Encyclopedia of Cancer, 1938–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_2477.

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Naor, Zvi, and Rony Seger. "Gonadotropin-Releasing Hormone." In Encyclopedia of Cancer, 1577–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2477.

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Colao, Annamaria, and Claudia Pivonello. "Gonadotropin Releasing Hormone (GnRH)." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5110-1.

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Helvacioglu, A. "Gonadotropin Releasing Hormone Treatment." In New Trends in Reproductive Medicine, 176–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60961-9_17.

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Colao, Annamaria, and Claudia Pivonello. "Gonadotropin Releasing Hormone (GnRH)." In Endocrine Pathology, 339–40. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5110.

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Shulman, Dorothy I., and Barry B. Bercu. "Molecular Biology of Gonadotropin-Releasing Hormone and the Gonadotropin-Releasing Hormone Receptor." In Molecular and Cellular Pediatric Endocrinology, 179–89. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-697-3_10.

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Siler-Khodr, T. M. "Human Chorionic Gonadotropin-Releasing Hormone." In Gynecology and Obstetrics, 837–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70559-5_281.

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Rivier, J., S. Koerber, J. Porter, C. Rivier, C. Hoeger, S. Struthers, M. Perrin, et al. "Characterization of Gonadotropin Hormone-Releasing Hormone Analogs." In Methods in Protein Sequence Analysis, 329–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73834-0_44.

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Conference papers on the topic "Gonadotropin releasing hormone"

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Ohlsson, M., A. J. W. Hsueh, and T. Ny. "HORMONE REGULATION OF THE FIBRINOLYTIC SYSTEM IN THE OVARY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644389.

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In the ovary, the release of oocytes from graafian follicles during hormone-induced ovulation has been found to be associated with substantial increases in follicular plasminogen activator (PA) activity. Most of the PA activity comes from the granulosa cells that have been shown to produce tPA, uPA as well as the type-1 PA-inhibitor,(PAI-1).We have studied the molecular mechanism of follicle stimulating hormone (FSH) and gonadotropin releasing hormone (GnRH) on the synthesis of tPA in primary cultures of rat granulosa cells. FSH and GnRH were both found to induce tPA in granulosa cells in a time and dose dependent manner. The effect of FSH and GnRH on the levels of tPA mRNA was also studied by northern and slot blot hybridizations. FSH and GnRH were both found to increase the level of tPA mRNA. The stimulation was up to 18 -fold compared to untreated cells.The induction of tPA mRNA by FSH and GnRH was additive and the time courses of the stimulation by the hormones differed, suggesting that different cellular mechanisms are involved. Consistent with the ability of FSH to activate the cAMP dependent protein kinase A pathway, the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine further enhanced the FSH induction of tPA mRNA.GnRH is known to activate the phospholipid-dependent protein kinase C pathway. Likewise the effect of GnRH can be mimicked by the kinase C activator, phorbol myristate acetate.It is concluded that FSH and GnRH regulates tPA production by differnt molecular mechanisms, and that the increase in tPA activity is mediated via an increase in the levels tPA mRNA. Since both gonadotropins and GnRH cause ovulation in hyposectomized animals, similar stimulatory actions of these hormones on the tPA activity suggest a correlative relationship between this enzyme and the ovulatory process.
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"TOWARDS A NEW HOMOGENEOUS IMMUNOASSAY FOR GONADOTROPIN-RELEASING HORMONE BASED ON TIME-RESOLVED FLUORESCENCE ANISOTROPY." In International Conference on Biomedical Electronics and Devices. SciTePress - Science and and Technology Publications, 2011. http://dx.doi.org/10.5220/0003152001840188.

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Bibiari, Georgia, Agathi Nteli, Carmen Simal, Christos Markatos, Vlasios Karageorgos, Alexios Vlamis-Gardikas, George Liapakis, and Theodore Tselios. "Design and Synthesis of Gonadotropin Releasing Hormone (GnRH) Peptide Analogues Conjugated with Anthraquinone for Selective Immunosuppression." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps.2022.065.

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Biniari, Georgia, Agathi Nteli, Carmen Simal, Christos Markatos, Vlasios Karageorgos, Alexios Vlamis-Gardikas, George Liapakis, and Theodore Tselios. "Design and Synthesis of Gonadotropin Releasing Hormone (GnRH) Peptide Analogues Conjugated with Anthraquinone for Selective Immunosuppression." In 36th European Peptide Symposium. The European Peptide Society, 2022. http://dx.doi.org/10.17952/36eps/36eps.2022.065.

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Pacucci, VA, F. Ceccarelli, G. Perrone, I. Zannini, M. Candelieri, I. Leccese, C. Perricone, et al. "SAT0260 Ovarian function preservation with gonadotropin-releasing hormone analogues in patients with systemic lupus erythematosus treated with cyclophosphamide." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6381.

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Kim, HJ, MH Lee, JE Lee, SH Park, ES Lee, Y.-J. Kang, JH Lee, et al. "Abstract P1-12-09: The oncologic effect of a gonadotropin releasing hormone (GnRH) agonist for ovarian protection during breast cancer chemotherapy." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p1-12-09.

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Yoon, TI, HJ Kim, JH Yu, G. Sohn, BS Ko, JW Lee, BH Son, and SH Ahn. "Abstract P5-13-06: Concurrent gonadotropin-releasing hormone (GnRH) agonist administration with chemotherapy improves neoadjuvant chemotherapy responses in young premenopausal breast cancer patients." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-13-06.

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Kim, Migang, Min chul Choi, Kwang-Beom Lee, Seok Mo Kim, Jung-Yun Lee, Jae-Hoon Kim, Jeong-Won Lee, et al. "Gonadotropin-releasing hormone (GnRH) agonist for prevention of chemotherapy induced menopause in malignant ovarian germ cell tumor: a multicenter prospective study (KGOG-3048)." In KSGO 2023. Korea: Korean Society of Gynecologic Oncology, 2023. http://dx.doi.org/10.3802/jgo.2023.34.s1.tip10.

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Sand, Sharon R., Catherine Klifa, Michael F. Press, Malcolm Pike, Giske Ursin, Darcy Spicer, Lalit Vora, et al. "Abstract 3557: Reduced ovarian hormones & reduced mammographic & MRI determined breast density inBRCAcarriers following a hormonal chemo-prevention regimen of gonadotropin releasing hormone agonist (GnRHA) & low-dose add-back estrogen & testosterone." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3557.

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Kim, H., W. Lim, E. Park, J. Sei, B. Koh, B. Son, S. Kim, et al. "Adriamycin and cyclophosphamide followed by tamoxifen, versus the combination of gonadotropin-releasing hormone analog and tamoxifen, in the treatment of premenopausal endocrine-responsive node-negative breast cancer." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-1151.

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Reports on the topic "Gonadotropin releasing hormone"

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Xu, Dan, Xueying Zhou, Junfei Wang, Xi Cao, and Tao Liu. The Value of Urinary Gonadotropins in the Diagnosis of Central Precocious Puberty: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0076.

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Review question / Objective: Precocious puberty is defined as the onset of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys. It can be differentiated into central precocious puberty (CPP) and peripheral precocious puberty, and it is more common in girls than in boys. CPP may result in a decreased final adult height, an early age at menarche, and psychological and health problems in adulthood. Gonadotropin-releasing hormone (GnRH) GnRH stimulation test has been indispensable in the diagnosis of CPP. GnRH stimulation test is not only invasive, time-consuming and expensive, but also sometimes difficult to have patients cooperate. Nocturnal urinary LH and FSH can represent gonadotropin excretion in children with normal and early puberty. And urinary sample collection and evaluation are more convenient, more acceptable, cheaper, and noninvasive. This meta-analysis aims to assess the value of first-voided urinary luteinizing hormone (LH) and the ratio of urinary luteinizing hormone and follicle-stimulating hormone (FSH) in the diagnosis of female CPP and to compare the accuracy between urinary gonadotropins and serum GnRH-stimulated gonadotropins.
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Gu, Li, Xurui Li, and Wentao Liu. Adverse cardiovascular effect following Gonadotropin-releasing Hormone (GnRH) antagonist versus GnRH agonist for Prostate Cancer Treatment: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0009.

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Zohar, Yonathan, Robert Langer, Shimon Hassin, Walton Dickhoff, Abigail Elizur, and Yoav Gothilf. A Novel Technology for the Manipulation of Fish Reproductive Cycles: Controlled Release of Gonadotropin Releasing Hormones. United States Department of Agriculture, March 1993. http://dx.doi.org/10.32747/1993.7603811.bard.

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Yaron, Zvi, Abigail Elizur, Martin Schreibman, and Yonathan Zohar. Advancing Puberty in the Black Carp (Mylopharyngodon piceus) and the Striped Bass (Morone saxatilis). United States Department of Agriculture, January 2000. http://dx.doi.org/10.32747/2000.7695841.bard.

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Both the genes and cDNA sequences encoding the b-subunits of black carp LH and FSH were isolated, cloned and sequenced. Sequence analysis of the bcFSHb and LHb5'flanking regions revealed that the promoter region of both genes contains canonical TATA sequences, 30 bp and 17 bp upstream of the transcription start site of FSHb and LHb genes, respectively. In addition, they include several sequences of cis-acting motifs, required for inducible and tissue-specific transcriptional regulation: the gonadotropin-specific element (GSE), GnRH responsive element (GRE), half sites of estrogen and androgen response elements, cAMP response element, and AP1. Several methods have been employed by the Israeli team to purify the recombinant b subunits (EtOH precipitation, gel filtration and lentil lectin). While the final objective to produce pure recombinantGtH subunits has not yet been achieved, we have covered much ground towards this goal. The black carp ovary showed a gradual increase in both mass and oocyte diameter. First postvitellogenic oocytes were found in 5 yr old fish. At this age, the testes already contained spermatozoa. The circulating LH levels increased from 0.5 ng/ml in 4 yr old fish to >5ng/ml in 5 yr old fish. In vivo challenge experiments in black carp showed the initial LH response of the pituitary to GnRH in 4 yr old fish. The response was further augmented in 5 yr old fish. The increase in estradiol level in response to gonadotropic stimulation was first noted in 4 yr old fish but this response was much stronger in the following year. In vivo experiments on the FSHb and LHb mRNA levels in response to GnRH were carried out on common carp as a model for synchronom spawning cyprinids. These experiments showed the prevalence of FSHP in maturing fish while LHP mRNA was prevalent in mature fish, especially in females. The gonadal fat-pad was found to originate from the retroperitoneal mesoderm and not from the genital ridge, thus differing from that reported in certain amphibians This tissue possibly serves as the major source of sex steroids in the immature black carp. However, such a function is taken over by the developing gonads in 4 yr old fish. In the striped bass, we described the ontogeny of the neuro-endocrine parameters along the brain-pituitary-gonadal axis during the first four years of life, throughout gonadal development and the onset of puberty. We also described the responsiveness of the reproductive axis to long-term hormonal manipulations at various stages of gonadal development. Most males reached complete sexual maturity during the first year of life. Puberty was initiated during the third year of life in most females, but this first reproductive cycle did not lead to the acquisition of full sexual maturity. This finding indicates that more than one reproductive cycle may be required before adulthood is reached. Out of the three native GnRHs present in striped bass, only sbGnRH and cGnRH II increased concomitantly with the progress of gonadal development and the onset of puberty. This finding, together with data on GtH synthesis and release, suggests that while sbGnRH and cGnRH II may be involved in the regulation of puberty in striped bass, these neuropeptides are not limiting factors to the onset of puberty. Plasma LH levels remained low in all fish, suggesting that LH plays only a minor role in early gonadal development. This hypothesis was further supported by the finding that experimentally elevated plasma LH levels did not result in the induction of complete ovarian and testicular development. The acquisition of complete puberty in 4 yr old females was associated with a rise in the mRNA levels of all GtH subunit genes, including a 218-fold increase in the mRNA levels of bFSH. mRNA levels of the a and PLH subunits increased only 11- and 8-fold, respectively. Although data on plasma FSH levels are unavailable, the dramatic increase in bFSH mRNA suggests a pivotal role for this hormone in regulating the onset and completion of puberty in striped bass. The hormonal regulation of the onset of puberty and of GtH synthesis and release was studied by chronic administration of testosterone (T) and/or an analog of gonadotropin-releasing hormone (G). Sustained administration of T+G increased the mRNA levels of the PLH subunit to the values characteristic of sexually mature fish, and also increased the plasma levels of LH. However, these changes did not result in the acceleration of sexual maturation. The mRNA levels of the bFSH subunit were slightly stimulated, but remained about 1/10 of the values characteristic of sexually mature fish. It is concluded that the stimulation of FSH gene expression and release does not lead to the acceleration of sexual maturity, and that the failure to sufficiently stimulate the bFSH subunit gene expression may underlie the inability of the treatments to advance sexual maturity. Consequently, FSH is suggested to be the key hormone to the initiation and completion of puberty in striped bass. Future efforts to induce precocious puberty in striped bass should focus on understanding the regulation of FSH synthesis and release and on developing technologies to induce these processes. Definite formulation of hormonal manipulation to advance puberty in the striped bass and the black carp seems to be premature at this stage. However, the project has already yielded a great number of experimental tools of DNA technology, slow-release systems and endocrine information on the process of puberty. These systems and certain protocols have been already utilized successfully to advance maturation in other fish (e.g. grey mullet) and will form a base for further study on fish puberty.
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