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1

Weaver, Richard Emyr. "Ligand-receptor interactions at the parathyroid hormone receptors." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531595.

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2

Göthe, Sten. "Life without thyroid hormone receptors /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-507-7/.

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3

Hussein, Mohamed Osman. "Hormonal modulation of Leydig cell membrane luteinizing hormone receptors /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487267024995937.

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4

Beeren, Hermina Catharina van. "Amiodarone and thyroid hormone receptors." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/71850.

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5

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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6

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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7

馬智謙 and 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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8

Zheng, Jianfei. "Development of thyroid hormone receptor-targeting conjugates." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 130 p, 2009. http://proquest.umi.com/pqdweb?did=1833641661&sid=5&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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9

Nawaz, Zafar. "Molecular Mechanism of Action of Steroid Hormone Receptors." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc798398/.

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A novel bacterial expression system that is capable of producing high levels of soluble, stable, biologically active human vitamin D3 and estrogen receptors has been developed. The method utilizes ubiquitin fusion technology and a low temperature nalidixic acid induction of the lambda PL promoter. This system can produce large quantities of receptor antigen, but only a small fraction displays wild-type DNA and hormone binding properties. Therefore, the use of this system to overproduce receptors for crystallization studies is not practical. To overcome these problems, a 2 um based ubiquitin fusion system which allows regulated expression of the estrogen receptor in yeast (Saccharomyces cerevisiae) was developed. This system produces the estrogen receptor to a level of 0.2% of the total soluble protein. Moreover, this protein is undegradable, soluble, and biologically active. To test the transcriptional activity of the estrogen receptor produced in yeast, a cis-trans transcription assay was developed. This assay revealed that the transcriptional activity of the human estrogen receptor expressed in yeast was similar to that observed in transfected mammalian cells. This reconstituted estrogen transcription unit in Saccharomyces cerevisiae was utilized to examine the regulation of estrogen receptor functions by antiestrogens, to develop a random and rapid approach for identifying novel estrogen response elements, to characterize estrogen receptor variants cloned from human breast tumors, and to examine the effect of estrogen receptor on the regulation of osteocalcin gene.
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10

Hassan, A. Quamrul. "Molecular complementation of mutant thyroid hormone receptors that disrupt transactivation mechanism." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 9.11 Mb., 175 p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3205433.

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11

Dunn, Erin Kristine. "Endothelial nuclear hormone receptors in atherosclerosis." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3402333.

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Thesis (Ph. D.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed May 19, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (leaves 50-56).
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12

Gullberg, Hjalmar. "Thyroid hormone receptors in liver metabolism /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-190-x/.

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13

McGinley, Paula Lynn. "Molecular complementation of mutant hormone receptors." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 189 p, 2008. http://proquest.umi.com/pqdweb?did=1456289611&sid=5&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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14

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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15

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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16

Schoenfeld, Vincent. "Isolation and characterisation of nuclear hormone receptors." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627546.

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17

Subramanian, Kelly Sue. "Nuclear Export Dynamics of Thyroid Hormone Receptors." W&M ScholarWorks, 2012. https://scholarworks.wm.edu/etd/1539626924.

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18

Mansén, Anethe. "Gene regulation by nuclear hormone receptors in vivo /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-678-2.

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19

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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20

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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21

Kabeer, Muhammad Asif. "The immunohistochemical evaluation of thyroid hormone and growth hormone receptors in colorectal carcinoma." Thesis, University of Exeter, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.530383.

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22

Hild-Petito, Sheri Ann. "Distribution of estrogen and progesterone receptors in the primate ovary, with emphasis on subpopulations of cells within the corpus luteum." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184485.

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Both estradiol and progeterone are proposed autocrine or paracrine regulators of ovarian function in primate species. However, specific receptors for these steroids have not been localized to individual compartments of the primate ovary. Using immunocytochemical techniques, estradiol receptors were detected in the germinal epithelium, but not other structures, of ovaries obtained from rhesus or cynomolgus monkeys during the follicular and luteal phases of the menstrual cycle. In contrast, progesterone receptors were present in stromal and interstitial tissue, the thecal layers of healthy and atretic follicles, as well as the functional corpus luteum. These results are consistent with the concept of a receptor-mediated role for progesterone, but not estrogen, within the predominant gametogenic and endocrine structures, e.g., the follicle and corpus luteum, of the primate ovary. The recent discovery of distinct cell types in the corpus luteum of domestic ungulates has revised concepts on the control of luteal function in these species. Studies were designed to test the hypothesis that the primate corpus luteum consists of cell subpopulations that differ in physical characteristics, function and regulation. Cells enzymatically-dispersed from the monkey corpus luteum at mid-luteal phase of the menstrual cycle differed in size (diameter) and the presence of the steroidogenic enzyme, 3β-hydroxysteroid dehydrogenase (3β-HSD). Analysis of dispersed cells for forward and 90° light scatter properties by flow cytometry revealed two distinct continua (Cα and Cβ). These continua were isolated using the sorting capabilities of the flow cytometer. Cα contained single cells of ≤ 15 μm and cell clusters; the cells were typically 3β-HSD-negative nonsteroidogenic. Cβ consisted of single cells that increased in size up to 40 μm and were 3β-HSD-positive. Cβ was divided into two regions (R₁ and R₃) and the cells isolated. R₁ cells were ≤ 15 μm whereas R₃ cells were ≥ 20 μm. Basal progesterone and estrogen production by R₃ cells was greater than that produced by R₁ cells (as determined by radioimmunoassay of the incubation media). Relative stimulation of progesterone production by hCG, cAMP or PGE₂ was not different between R₁ and R₃ luteal cells. These results support the hypothesis that the primate corpus luteum consists of distinct cell subpopulations which differ in size and steroidogenic capacity. However, the cell types which secrete progesterone are typically responsive to gonadotropin and PGE₂, possibly via a cAMP-mediated pathway.
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23

Beaumont, Timothy Martin. "Regulation of stress hormone receptors in fish cells." Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366436.

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24

Rahmani, Hamid Reza. "Neurohypophyseal hormone receptors in the female ovine brain." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337294.

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25

Moss, Catherine Elizabeth. "G-protein coupled receptors modulating incretin hormone secretion." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648611.

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26

Lau, Suk-ling Joanna, and 劉淑玲. "Molecular characterization of the chicken growth hormone receptorgene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45015430.

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27

Moran, Carla. "Characterisation of resistance to thyroid hormone mediated by defective thyroid hormone receptor [beta] or [alpha]." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708931.

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28

Hess-Wilson, Janet Katherine. "Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168452681.

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29

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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30

Deng, Luqin. "Determinants of growth hormone receptor downregulation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009p/deng.pdf.

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31

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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32

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.
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33

Mabrouka, Maamra Bent Ahmed Ben Laid. "Truncated cytokine receptors and antagonists : signalling and trafficking." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251278.

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34

Nygård, Maria. "Regulation of gene transcription by the thyroid hormone receptors /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-756-1/.

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35

Abu, Emmanuel Ogbole. "The expression of thyroid hormone receptors in human bone." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624713.

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36

Cziko, Paul. "Molecular Physiological Evolution: Steroid Hormone Receptors and Antifreeze Proteins." Thesis, University of Oregon, 2015. http://hdl.handle.net/1794/18733.

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For my dissertation research I explored the diversity and functional evolution of steroid hormone receptors (SRs) in animals and the physiological implications of the evolution of antifreeze proteins in Antarctic notothenioid fishes. For the former, I discovered multiple new SRs from the vast and under-sampled swath of animal diversity known as invertebrates. I used the sequences of these and other newly discovered related receptors in combination with genomic data and molecular phylogenetic techniques to revise the understanding of the evolutionary history of this important gene family. While previous studies have suggested that vertebrate SR diversity arose from a gene duplication in an ancestor of all bilaterian animals, my work presents strong evidence that this duplication occurred much later, at the base of the chordates. Furthermore, to determine the implications of added diversity and a revised phylogeny on inferences of the functional evolution of SRs, I functionally characterized heretofore-unknown SRs from hemichordates, an acoelomate flatworm, and a chaetognath and statistically reconstructed and functionally characterized ancestral SRs. My results expand the known sequence and functional repertoire of SRs in animals while reinforcing the previous inference that all SRs evolved from an estrogen-sensitive ancestral receptor. I also explored the consequences of the evolution of antifreeze proteins in Antarctic notothenioid fishes, a crucial adaptation to their icy, polar environment. These special proteins adsorb to ice crystals that enter a fish's body and prevent further growth, thereby averting death. I discovered that, in addition to their lifesaving growth-inhibiting ability, AFPs also prevent the melting of internal ice crystals at temperatures above the expected equilibrium melting point. Together with a decade-long temperature record of one of the coldest fish habitats on earth, my experimental results show that the evolution and expression of antifreeze proteins is accompanied by a potentially detrimental consequence: the lifelong accumulation of ice inside these fishes' bodies. This dissertation includes previously published co-authored material as well as unpublished co-authored material.
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37

Wang, Ying, and 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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Harding, Ruth Linda Paulina. "Characterization and purification of receptors for growth hormone in normal and growth hormone-treated ruminants." Thesis, University of Sussex, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235532.

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39

Wormald, Patricia J. "GnRH and neuropeptide regulation of gonadotropin secretion from cultured human pituitary cells." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27168.

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Gonadotropin-releasing hormone (GnRH) and its superactive analogues are currently being used in the treatment of a number of endocrine disorders, such as endometriosis, precocious puberty, infertility and prostatic cancer. Selection of these analogues for clinical use have been previously based on their activities in animal models. This thesis has therefore investigated the binding characteristics of the human GnRH receptor, in comparison to those of the rat receptor, as well as the activities of a number of GnRH analogues for stimulating luteinising hormone (LH) and follicle stimulating hormone (FSH) secretion from cultured human pituitary cells. The establishment of a human pituitary bioassay system has further made possible the investigation of the direct regulatory roles of GnRH and other neuropeptides in man. To date, such studies in man have been performed in vivo and are thus complicated by the simultaneous interactions of numerous modulators.
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40

Hoo, L. C., and 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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潘建基 and Kin-kee Pun. "Functional and structural characterization of parathyroid hormone receptors in health and disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B31231664.

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42

Jetson, Rachael Rene. "Design and Development of Potential Therapeutic Agents for Use in Hormone Responsive Cancers." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1384270219.

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43

Sun, Caiyun. "Luteinizing hormone receptor and its functional role in gonadotropin-induced growth hormone gene transcription in grass carp." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39556967.

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孫彩云 and Caiyun Sun. "Luteinizing hormone receptor and its functional role in gonadotropin-induced growth hormone gene transcription in grass carp." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39556967.

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45

Wihlbäck, Anna-Carin. "Ovarian hormones and effects in the brain : studies of neurosteroid sensitivity, serotonin transporter and serotonin2A receptor binding in reproductive and postmenopausal women." Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-365.

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46

Feng, Xiaopeng. "Chicken growth hormone receptor and growth hormone : search for genetic variants which affect commercially important traits." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42028.

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Chicken genomic DNA containing 5 kb of the 5$ sp prime$ end of the growth hormone (GH) receptor gene and 12 kb of the region up-stream was cloned and a restriction map was constructed. Using subcloned fragments as probes, a HindIII polymorphism was detected in both egg layer and in meat-type chickens. This polymorphic site was mapped at 7 kb up-stream of the coding region of the GH-receptor gene and a PCR assay for the polymorphism was developed to facilitate genotyping of large numbers of chickens.
Alleles of the GH-receptor gene and the GH gene were analyzed for association with traits in chicken strains of different genetic origins. In egg layers, association was significant for juvenile body weight, egg weight, feed consumption and feed efficiency for egg mass (P $<$ 0.05). In meat-type chickens, the GH-receptor allele associated with high juvenile body weight in egg layers was co-selected with leanness. A comparison of the genotype classes revealed that for several traits there was significant interaction between the GH and GH-receptor genotype. The results indicated that there are variants of the genes of the GH-axis which affect traits in White Leghorns and that the effect of a genetic variation in one gene may depend on the variation in another gene.
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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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48

ALLEGRETTO, ELIZABETH ANNE. "STRUCTURE - FUNCTION RELATIONSHIPS OF THE VITAMIN D HORMONE RECEPTOR." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184182.

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Avian intestinal cytosoluble receptors for 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) were subjected to limited trypsin digestion, endogenous proteolytic action, as well as carboxypeptidase treatment, and the physical and functional properties of the resulting discrete polypeptide fragments were identified and contrasted with the native 1,25(OH)₂D₃ receptor. Resultant fragments were followed by tracing either radioactive 1,25(OH)₂D₃ or by probing with anti-receptor monoclonal antibodies. Two differentially trypsin-sensitive effects on the 1,25(OH)₂D₃ receptor were noted when fragments were detected by their ability to bind 1,25(OH)₂[³H]D₃. Two hormone-bound fragments of 40 and 30 kDa were formed; neither bound to DNA-cellulose nor anti-receptor monoclonal antibodies. Immunoblot technology was used to show the disappearance of the 60 kDa receptor with increasing trypsin concentrations, paralleling the appearance of an immunoreactive 20 kDa fragment. The 20 kDa fragment did not bind hormone but was capable of interacting with DNA-cellulose in a fashion identical to that of the 60 kDa receptor. This fragment is likely the complementary fragment to the hormone-bound fragment of 40 kDa that is described above. In contrast to the exogeneous effect of trypsin, incubation of chick intestinal cytosol resulted in the time-dependent formation of an endogenous protease-derived fragment of 45 kDa. This species retained the hormone-binding site and the antibody determinant, but was devoid of DNA-binding activity. Moreover, it did not generate the trypsin-dependent 20 kDa fragment and therefore was derived from the opposite end of the receptor molecule. Carboxypeptidase treatment of the 1,25(OH)₂D₃ receptor produces a 56 kDa fragment which does not retain hormone, but which does bind to DNA-cellulose and monoclonal antibody. These combined data from various limited enzymatic cleavage studies of the receptor have facilitated the construction of a schematic model of the chick receptor in which the immunoreactive epitope is located between the N-terminal DNA-binding domain and the C-terminal hormone-binding domain. This map for the 1,25(OH)₂D₃ receptor protein is consistent with the general structure of steroid and thyroid hormone receptors and places the vitamin D hormone receptor in a class of macromolecules that are postulated to bind enhancer regions of responsive DNA and thereby control target gene transcription.
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49

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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50

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.
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