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1 hGH expression was evaluated by in situ hybridization an
2 hGH variants were chosen to probe different features of
3 hGH was also expressed in parvocellular neurones in supr
4 alanine substitutions were determined for 35 hGH(v) residues that are directly contained in or closel
6 r hGH locus histone acetylation and activate hGH-N transcription from an inactive locus, we expressed
10 conditional deletion of HSI from the active hGH locus in the adult pituitary effectively silences hG
14 eveloped to measure the kinetics for hPL and hGH binding to the hPRLR ECD, with and without Zn2+ and
15 residues that are identical between hPL and hGH contribute quite differently to the binding of the h
17 n of histone hyperacetylation at the LCR and hGH-N promoter in these cells similar to that observed i
20 veral techniques to detect the specific anti-hGH antibodies using indirect immunoassay format on the
21 chip has been shown to detect specific anti-hGH antibodies using the combination of three different
23 without hyperglycemia and a decrease in both hGH synthesis and secretion, but no difference in endoge
25 for ND in recipients of pituitary-derived c-hGH by reviewing the National Hormone and Pituitary Prog
27 c-related disease, this population of NHPP c-hGH recipients does not appear to be at increased risk o
28 l sclerosis (ALS) were found among US NHPP c-hGH recipients, including 2 of the 796 decedents in the
29 Despite the likely frequent exposure of c-hGH recipients to NDAPs, and their markedly elevated ris
30 ALS cases of unclear significance among US c-hGH recipients despite the absence of pathological depos
33 her Pit-1 expression is sufficient to confer hGH locus histone acetylation and activate hGH-N transcr
36 th a hypoxia mimetic significantly decreased hGH RNA levels and was accompanied by recruitment of HIF
37 d constitutive secretion of hGH and depleted hGH stores in secretory vesicles, GTP-bound Rab11b only
38 the hGH locus that is associated with distal hGH-N activation, and the discrete determinants of this
39 I hypersensitive site I (HSI), the dominant hGH LCR element, is separated from the hGH-N promoter by
44 the C-terminal domains of two receptor ECDs (hGH(R1)- hGH(R2)) are conserved; however, the large chan
45 SII in conjunction with HSI further enhanced hGH-N transgene expression, indicating additional determ
46 b); and the 3'-border included the expressed hGH-N gene, but did not extend farther 3' into the place
48 epitope with that previously determined for hGH indicates contributions of individual residues track
49 e placentas of mouse embryos carrying a full hGH cluster to that in placentas in which the HSIII-HSV
55 sed transgenic mice expressing the human GH (hGH) gene, GH1, to assess the effect of high caloric int
56 o human growth hormone (hGH) (Thr175 --> Gly-hGH) and the extracellular domain of the hGH receptor (T
61 gh-affinity variant of human growth hormone (hGH(v)) contains 15 mutations within site 1 and binds to
62 ations introduced into human growth hormone (hGH) (Thr175 --> Gly-hGH) and the extracellular domain o
63 distinct locations in human growth hormone (hGH) allowed site-specific conjugation with polyethylene
64 highly conserved with human growth hormone (hGH) and both hormones bind to the hPRLR extracellular d
67 conducting studies on human growth hormone (hGH) and pyrin domain (PYD), and the results show how mu
68 nity Site 1 variant of human growth hormone (hGH) and two copies of the extracellular domain (ECD) of
69 at express transfected human growth hormone (hGH) as a secreted reporter protein, we have searched fo
71 ng site (Site1) of the human growth hormone (hGH) binds to its cognate receptor (hGHR) via a concave
72 The five genes of the human growth hormone (hGH) cluster are expressed in either the pituitary or pl
77 ific activation of the human growth hormone (hGH) gene cluster in the pituitary and placenta constitu
79 mmunoassay format with human growth hormone (hGH) immobilized on the self-assembled monolayer (SAM) m
81 owth hormone loci, the human growth hormone (hGH) locus is regulated by a distal locus control region
85 xtracellular domain of human growth hormone (hGH) receptor, and the intracellular domain of GLM-R.
86 nsactivate the genomic human growth hormone (hGH) reporter construct in the absence of a driving test
88 G binding with that of human growth hormone (hGH) to its receptor (hGH-R) which displays an invariant
89 in vivo analysis of a human growth hormone (hGH) transgene locus, we report that activation of a dom
90 inding of a variety of human growth hormone (hGH) variants to the human growth hormone receptor (hGHR
92 similarity of hPRL to human growth hormone (hGH), a member of the same family as hPRL, where the MBS
95 , interleukin-4 (IL4), human growth hormone (hGH), and prolactin (PRL) all form four-helix bundles an
97 ak self-association of human growth hormone (hGH, KD = 0.90 +/- 0.03 mM) at neutral pH by the paramag
102 nglycosylated protein (human growth hormone [hGH]) that was secreted equally from both surfaces.
106 he basal rate constants (k(a0)) of EPO, IL4, hGH, and PRL were similar (5.2 x 10(5) M(-1)s(-1), 2.4 x
110 A significant and dose-dependent decrease in hGH and mouse GH RNA levels was detected in primary pitu
112 a role for Pit-1 as an initiating factor in hGH locus activation during somatotrope ontogeny, acting
113 ion of HSII, expanding the role of POU1F1 in hGH LCR activity, and provide insight on the molecular e
114 hether the closely linked HSII has a role in hGH-N expression, it was deleted from a previously valid
116 the PREs of the amide protons at increasing hGH concentrations and a constant concentration of the r
118 ehensive phi analysis showed that individual hGH interface residues do not contribute energetically t
121 cells, transgenic mice expressing the intact hGH locus in a somatotroph-specific manner were generate
124 e latter residues increase only at the lower hGH concentrations but decrease at the higher concentrat
125 acetylated domain coincided with the 5' most hGH LCR element, HSV (-34 kb); and the 3'-border include
127 hosphorylation assays showed that the mutant hGH activates growth hormone signaling in the presence o
136 This was accompanied by the activation of hGH-N transcription and an increase in intergenic and CD
138 ppears that the improved binding affinity of hGH(v) site 1 was not achieved through minor adjustments
139 t is found that the ultraweak aggregation of hGH involves several interaction sites that are located
142 dies confirm and expand reported benefits of hGH therapy in children with PWS, including a possible s
144 y interactions that inhibited the binding of hGH(wt) are replaced by interactions that make positive
146 roduced a set of mutations on the complex of hGH with its receptor that putatively enhances the rate
148 at -14.5 kb, is the dominant determinant of hGH-N expression and is essential for establishment of a
149 ar to cause global changes in the domains of hGH(R1) that affect the hGH(v)-hGH(R2) interface indirec
151 the level of transcriptional enhancement of hGH-N by HSI is directly related to the intensity of HSI
155 ing hypothesis is that the catalytic fold of hGH is similar to the folding of this domain in carbamoy
163 -triggered exocytosis by causing the loss of hGH from the PC12 cells, whereas GTP-bound Rab11b direct
168 xpression of DA-Rab11a stimulated release of hGH into the bladder lumen, expression of DN-Rab11a had
169 GH1) locus to investigate the rhythmicity of hGH synthesis and secretion and to show that RNA and sec
171 greatly stimulated constitutive secretion of hGH and depleted hGH stores in secretory vesicles, GTP-b
174 ind specifically to either Site1 or Site2 of hGH, providing novel reagents for biophysical and biolog
178 structure with the 1:1 complex structure of hGH bound to the hPRLR ECD1 suggests that two surface lo
180 ble for the first time to detect variants of hGH with very weak affinities for the hGHbp (K(d)>1 micr
184 icating additional determinants of pituitary hGH-N activation in the HSII region, but limitations of
186 serve that a major function of the placental hGH LCR is to insulate the transgene locus from site-of-
187 ate that energy homeostasis alters postnatal hGH synthesis through dynamic changes in the 3-dimension
188 isol, estradiol, testosterone, progesterone, hGH and prolactin) and the obtained results demonstrated
189 minal domains of two receptor ECDs (hGH(R1)- hGH(R2)) are conserved; however, the large changes in Si
190 ing transcription adjacent to the long-range hGH-N enhancer, HSI, is established by the enhancer inde
191 In anaesthetised, water-loaded JP17 rats, hGH was released with VP in response to an acute hypovol
192 human growth hormone (hGH) to its receptor (hGH-R) which displays an invariant dissociation constant
194 to HSI was sufficient for properly regulated hGH-N expression in transgenic mice, while HSII alone ha
199 nohistochemistry and radioimmunoassay showed hGH protein in the hypothalamus from where it was transp
201 peak at HSI/II, the major pituitary-specific hGH LCR determinant (-15 kb), with gradually decreasing
208 se findings support previous assertions that hGH can reduce morbidity and improve function in childre
210 ease of platelet production, indicating that hGH may exert a complementary and synergistic effect wit
213 this study, we show for the first time that hGH has a distinct capacity to promote the differentiati
225 ncident with Pit-1 occupancy at HS-I and the hGH-N promoter and were observed irrespective of the bas
228 ol II) factories, histone acetylation at the hGH-N promoter, and looping of the LCR to its target pro
233 hat the entire 87 kb region encompassing the hGH LCR and contiguous hGH gene cluster was devoid of MA
237 es 3 and 4, while retaining affinity for the hGH receptor, we have engineered a new hGH variant (Q84C
238 inant hGH LCR element, is separated from the hGH-N promoter by a 14.5 kb span that encompasses the B-
239 odel in which the Pit-1 binding sites in the hGH LCR allosterically program the bound Pit-1 complex f
240 ut their contributions are attenuated in the hGH(v) interaction, and additional binding energy is acq
244 omic insert encompassing the majority of the hGH gene cluster and the entire contiguous LCR was estab
246 lish HSII as a nonredundant component of the hGH LCR essential for establishment of robust levels of
247 pport a model for bifunctional action of the hGH LCR in which separate positive determinants, HSI,II
250 ified to identify structural features of the hGH locus required for its appropriate placental express
251 These functions sustain engagement of the hGH locus with polymerase II (Pol II) factories, histone
252 ndicate that the unplanned expression of the hGH minigene in CollagenVI expressing mesenchymal cells
253 hese findings by analyzing the effect of the hGH minigene in TgC6hp55 transgenic mice which express t
254 ies of the extracellular domain (ECD) of the hGH receptor (hGHR) has been determined at 2.6 A resolut
255 Gly-hGH) and the extracellular domain of the hGH receptor (Trp104 --> Gly-hGHbp) created a cavity at
258 e employ a novel minichromosome model of the hGH-N regulatory domain and show that HSII confers robus
263 omain of histone acetylation targeted to the hGH locus that is associated with distal hGH-N activatio
264 coding transcription that is 'looped' to the hGH promoter as an essential step in initiating hGH gene
266 15 mutations within site 1 and binds to the hGH receptor (hGHR) approximately 400-fold tighter than
268 y-specific transcription factor Pit-1 to the hGH-N promoter and a selective decrease in promoter occu
269 , an LCR component located 14.5 kb 5' to the hGH-N promoter, constitutes the primary determinant of h
273 e former residues increase linearly with the hGH concentration in the entire concentration range beca
275 tributions of individual residues within the hGH(v) binding epitope and placed them in context with p
276 e POU1F1 binding to cognate sites within the hGH-LCR and hGH1 promoter, but not to sites within the P
279 inct sites: through its N-terminal domain to hGH, and to ECD1 through its C-terminal domain, which fo
282 ne for 72 h increased hypothalamic transgene hGH mRNA expression, and depleted posterior pituitary hG
283 two-step hormone-induced dimerization of two hGH receptors via their extracellular domains (ECDs).
296 acities (DeltaCp) on binding measured for wt-hGH and its variants are significantly larger than norma
297 (hGHv) and the wild-type growth hormone (wt-hGH) each binding to the extracellular domain of their r
298 e, a characteristic that was not found in wt-hGH or apparent in the temperature factor data from the
299 the hGHv molecule is less stable than its wt-hGH counterpart, its resulting active ternary complex wi
300 ery different thermodynamic partitioning: wt-hGH binding exhibits favorable enthalpy and entropy cont
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