ライフサイエンスコーパス: hGH

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

5 Concerns about hGH-associated sudden death persist, but recent studies

6 r hGH locus histone acetylation and activate hGH-N transcription from an inactive locus, we expressed

7 pecific transcriptional events that activate hGH-N also trigger ectopic activation of CD79b.

8 se Pit-1 elements are sufficient to activate hGH-N expression in the mouse pituitary.

9 ne acetylation that extends to and activates hGH-N in the pituitary gland.

10 conditional deletion of HSI from the active hGH locus in the adult pituitary effectively silences hG

11 tone acetylation that encompasses the active hGH locus.

12 When administering hGH nasally in rats with increasing concentrations of So

13 motropin genes (hCS-L, hCS-A, and hCS-B) and hGH-V, are expressed selectively in the placenta.

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

16 sidues track reasonably well between hPL and hGH.

17 n of histone hyperacetylation at the LCR and hGH-N promoter in these cells similar to that observed i

18 Several groups on hGH(v) and hGH(R2) undergo conformational changes of up to 8 A.

19 In the case of anti-hGH detection using pulsed amperometry (PA) with 3,3',5,

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

22 Significant similarity was found between hGH and the glutamine amidotransferase type I domain of

23 without hyperglycemia and a decrease in both hGH synthesis and secretion, but no difference in endoge

24 occurrence and severity are not increased by hGH exposure.

25 for ND in recipients of pituitary-derived c-hGH by reviewing the National Hormone and Pituitary Prog

26 decedents in the originally confirmed NHPP c-hGH cohort database.

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

31 tosis and caused an accumulation of cellular hGH.

32 We have previously cloned and characterized hGH cDNA and its gene.

33 her Pit-1 expression is sufficient to confer hGH locus histone acetylation and activate hGH-N transcr

34 gion encompassing the hGH LCR and contiguous hGH gene cluster was devoid of MAR activity.

35 In contrast, hGH expression is relatively low in spleen, lung, small

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

40 rts of improved cognitive development during hGH have also emerged.

41 mproved sleep cardiovascular function during hGH therapy.

42 However, the V(max) of the E222A hGH mutant was reduced only 6-fold relative to the wild-

43 ons and binds>10(2) tighter to the hGHR ECD (hGH(R1)) at Site 1.

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

47 To establish a mechanistic basis for hGH LCR function, we carried out acetylation mapping of

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

50 The five-gene hGH cluster is regulated by two partially overlapping se

51 single human pituitary growth hormone gene (hGH-N) and four placenta-specific paralogs.

52 Human growth hormone gene (hGH-N) expression is activated by an LCR marked by a ser

53 The human growth hormone gene (hGH-N) is regulated by a distal locus control region (LC

54 The human GH (hGH) gene cluster is regulated by a remote 5' locus cont

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

57 The H171N hGH mutant was found to have a 250-fold reduced V(max).

58 t also rendering a part of the alpha-helical hGH core slightly more dynamic.

59 0-fold tighter than does wild-type (wt) hGH (hGH(wt)).

60 ethylene glycol (PEG) to produce homogeneous hGH variants.

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

65 Human growth hormone (hGH) and bovine neurophysin (bNP) DNA reporter fragments

66 Using human growth hormone (hGH) and human leptin (hLeptin) as model proteins, we ha

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

70 Human growth hormone (hGH) binds lactogenic or somatotrophic receptors, creati

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

73 The human growth hormone (hGH) cluster contains five genes.

74 high affinity site of human growth hormone (hGH) for binding to its receptor (hGHR).

75 inity site (site 1) of human growth hormone (hGH) for binding to its receptor.

76 the pituitary-specific human growth hormone (hGH) gene and its locus control region (hGH LCR).

77 ific activation of the human growth hormone (hGH) gene cluster in the pituitary and placenta constitu

78 The human growth hormone (hGH) gene is controlled by a long-range enhancer, HSI, l

79 mmunoassay format with human growth hormone (hGH) immobilized on the self-assembled monolayer (SAM) m

80 Human growth hormone (hGH) is known to play a functional role in regulating he

81 owth hormone loci, the human growth hormone (hGH) locus is regulated by a distal locus control region

82 The human growth hormone (hGH) minigene used for transgene stabilization in mice h

83 The human Growth Hormone (hGH) multigene cluster contains five gene paralogs.

84 ng site driving either human growth hormone (hGH) or Cre recombinase genes.

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

87 Recombinant human growth hormone (hGH) therapy in children with Prader-Willi syndrome (PWS

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

91 Ectopic human growth hormone (hGH) was highly expressed in MIP-CreERT islets independe

92 similarity of hPRL to human growth hormone (hGH), a member of the same family as hPRL, where the MBS

93 but virally expressed human growth hormone (hGH), a secretory protein, was packaged into DFV.

94 Human growth hormone (hGH), and its receptor interaction, is essential for cel

95 , interleukin-4 (IL4), human growth hormone (hGH), and prolactin (PRL) all form four-helix bundles an

96 Signaling in the human growth hormone (hGH)-human GH receptor system is initiated by a controll

97 ak self-association of human growth hormone (hGH, KD = 0.90 +/- 0.03 mM) at neutral pH by the paramag

98 Human growth hormone (hGH-N) expression in the pituitary is under the regulati

99 Activation of the human growth hormone (hGH-N) gene in pituitary somatotropes is mediated by a l

100 The human pituitary growth hormone (hGH-N) locus is activated in the differentiating somatot

101 Expression of the human growth hormone (hGH-N) transgene in the mouse pituitary is dependent on

102 nglycosylated protein (human growth hormone [hGH]) that was secreted equally from both surfaces.

103 Human gamma-glutamyl hydrolase (hGH) is a central enzyme in folyl and antifolylpoly-gamm

104 Human gamma-glutamyl hydrolase (hGH) plays an important role in the metabolism of folic

105 0(4) M(-1)s(-1), respectively, for EPO, IL4, hGH, and PRL agree well with experimental results.

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

107 The model also predicted that His-171 in hGH may be involved in substrate binding.

108 yet resulted in a substantial loss (70%) in hGH-N mRNA expression.

109 Changes in hGH structure are unique when binding either lactogenic

110 A significant and dose-dependent decrease in hGH and mouse GH RNA levels was detected in primary pitu

111 There was no significant difference in hGH mRNA levels between breast cancer tissues and their

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

115 n several tissues, also leading to increased hGH protein levels in the serum.

116 the PREs of the amide protons at increasing hGH concentrations and a constant concentration of the r

117 Analysis of three independent hGH/P1(DeltaHSII) transgenic mouse lines revealed that t

118 ehensive phi analysis showed that individual hGH interface residues do not contribute energetically t

119 rom PC12 cells and nicotinic agonist-induced hGH release from bovine adrenal chromaffin cells.

120 promoter as an essential step in initiating hGH gene expression.

121 cells, transgenic mice expressing the intact hGH locus in a somatotroph-specific manner were generate

122 ethylation throughout the minichromosome LCR/hGH-N domain.

123 itutes the primary determinant of high-level hGH-N activation in pituitary somatotropes.

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

126 A mono-PEGylated mutant hGH modified at residue 35 demonstrated favorable pharma

127 hosphorylation assays showed that the mutant hGH activates growth hormone signaling in the presence o

128 r the hGH receptor, we have engineered a new hGH variant (Q84C/Y143C).

129 d on the conformational dynamics of this new hGH variant.

130 This model predicts that Cys-110 of hGH is the active site nucleophile and forms a catalytic

131 aling pathways are involved in the action of hGH.

132 ies essential for LCR-mediated activation of hGH in the developing pituitary.

133 HSI is essential for activation of hGH-N during pituitary development and for sustaining ro

134 nt mechanism for long-distance activation of hGH-N gene expression.

135 onfers robust POU1F1-dependent activation of hGH-N in this system.

136 This was accompanied by the activation of hGH-N transcription and an increase in intergenic and CD

137 D79b do not trigger reciprocal activation of hGH-N.

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

140 ence important to a benefit-risk analysis of hGH use in children with PWS.

141 Asp116 of hGH(v) plays a central role in the reorganization of Sit

142 dies confirm and expand reported benefits of hGH therapy in children with PWS, including a possible s

143 ake positive contributions to the binding of hGH(v).

144 y interactions that inhibited the binding of hGH(wt) are replaced by interactions that make positive

145 Comparison of hGH structures, either free or bound to a single lactoge

146 roduced a set of mutations on the complex of hGH with its receptor that putatively enhances the rate

147 The primary determinant of hGH LCR function maps to the pituitary-specific DNase I

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

150 ) mice, possibly due to paracrine effects of hGH-induced serotonin expression.

151 the level of transcriptional enhancement of hGH-N by HSI is directly related to the intensity of HSI

152 binding energy in the functional epitope of hGH(v) differs significantly from that of hGH(wt).

153 appeared to have heterogeneous expression of hGH mRNA.

154 High level expression of hGH was restricted to the pituitary and hCS to the labyr

155 ing hypothesis is that the catalytic fold of hGH is similar to the folding of this domain in carbamoy

156 its native site in B cells is independent of hGH LCR activity.

157 y and spatially concordant with induction of hGH-N in the embryonic pituitary.

158 In comparison, the interaction of hGH with the same receptor ECD did not demonstrate any s

159 define the three dimensional interactions of hGH with poly-gamma-glutamate substrates.

160 We report here that the levels of hGH gene expression are high in tissues such as liver, k

161 In addition, high levels of hGH mRNA were detected in most cancer cell lines examine

162 ential for establishment of robust levels of hGH-N gene expression.

163 -triggered exocytosis by causing the loss of hGH from the PC12 cells, whereas GTP-bound Rab11b direct

164 These data predict distinct modes of hGH cluster gene activation in the pituitary and placent

165 apical secretion of a glycosylated mutant of hGH that was secreted predominantly apically.

166 Additionally, several regions of hGH(v) structure move up to 9A in forming the interface.

167 rovide novel insights into the regulation of hGH gene transcription in HepG2 and MCF-7 cells.

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

170 those determined in the comparative scan of hGH to the hPRLR ECD1.

171 greatly stimulated constitutive secretion of hGH and depleted hGH stores in secretory vesicles, GTP-b

172 Using the sequence of hGH as a query, alignment searches of protein data bases

173 Here we generate a series of hGH/BAC transgenes specifically modified to identify str

174 ind specifically to either Site1 or Site2 of hGH, providing novel reagents for biophysical and biolog

175 -terminal domain of ECD2 binding to Site2 of hGH.

176 ng between the two receptor-binding sites of hGH.

177 del for the analysis of the full spectrum of hGH gene cluster activation.

178 structure with the 1:1 complex structure of hGH bound to the hPRLR ECD1 suggests that two surface lo

179 of hGH(v) differs significantly from that of hGH(wt).

180 ble for the first time to detect variants of hGH with very weak affinities for the hGHbp (K(d)>1 micr

181 Several groups on hGH(v) and hGH(R2) undergo conformational changes of up

182 In particular, hGH is potent in facilitating proplatelet formation and

183 H LCR in placental hCS, as well as pituitary hGH gene activation, and expression.

184 icating additional determinants of pituitary hGH-N activation in the HSII region, but limitations of

185 expression, and depleted posterior pituitary hGH and VP stores in parallel.

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

193 one (hGH) gene and its locus control region (hGH LCR).

194 to HSI was sufficient for properly regulated hGH-N expression in transgenic mice, while HSII alone ha

195 analyses were performed on 11 representative hGH Site1 variants that contained 14-20 mutations.

196 LCR blocks CD79b transcription and represses hGH-N expression.

197 ition-independent and somatotrope-restricted hGH-N transgene activation.

198 Immunogold electron microscopy showed hGH co-stored with VP-NP in the same granules.

199 nohistochemistry and radioimmunoassay showed hGH protein in the hypothalamus from where it was transp

200 in the adult pituitary effectively silences hGH-N expression.

201 peak at HSI/II, the major pituitary-specific hGH LCR determinant (-15 kb), with gradually decreasing

202 Both lines showed specific hGH expression in magnocellular VP cells in the hypothal

203 e predominant pituitary somatotrope-specific hGH-N activation function of the LCR.

204 Such spurious hGH transactivation also occurred upon co-transfection o

205 scription between this domain and the target hGH-N promoter.

206 ifferences compared to the wild-type ternary hGH hGHR complex.

207 fold higher affinity for the hPRLR ECD1 than hGH.

208 se findings support previous assertions that hGH can reduce morbidity and improve function in childre

209 This is the first evidence that hGH synthesis follows a diurnal rhythm and of dynamic as

210 ease of platelet production, indicating that hGH may exert a complementary and synergistic effect wit

211 The results reveal that hGH site 1 behaves in a highly additive manner and sugge

212 Studies consistently show that hGH improves stature, body composition, fat percentage a

213 this study, we show for the first time that hGH has a distinct capacity to promote the differentiati

214 The hGH binding interface is highly adaptable to mutations,

215 The hGH cluster contains a single human pituitary growth hor

216 The hGH gene is activated by a 5'-remote locus control regio

217 The hGH LCR mediates a domain of histone acetylation targete

218 The hGH mutants C110A, H220A, and E222A were prepared.

219 The hGH variant (hGH(v)) contains 15 Site 1 mutations and bi

220 The hGH(v) Site 1 interface is somewhat smaller and 20% more

221 The hGH(v)- hGH(R2) interface contains seven H-bonds, only o

222 The hGH-N gene is predominantly expressed in pituitary somat

223 The hGH-P8 fusion protein was found to be extremely tolerant

224 es in the domains of hGH(R1) that affect the hGH(v)-hGH(R2) interface indirectly.

225 ncident with Pit-1 occupancy at HS-I and the hGH-N promoter and were observed irrespective of the bas

226 re models to track structural changes at the hGH locus through placental-gene activation.

227 In contrast, Pit-1 sites at the hGH-N promoter are consistently unable to mediate simila

228 ol II) factories, histone acetylation at the hGH-N promoter, and looping of the LCR to its target pro

229 ic epigenetic modifications generated by the hGH LCR.

230 In contrast, the hGH-N transgene is not activated by Pit-1 sites native t

231 ctivated by Pit-1 sites native to either the hGH-N or rat (r)GH gene promoters.

232 ones H3 and H4 in chromatin encompassing the hGH cluster.

233 hat the entire 87 kb region encompassing the hGH LCR and contiguous hGH gene cluster was devoid of MA

234 d leptin-deficient obese mouse model for the hGH and hLeptin antibody fusions, respectively.

235 Further, they support a role for the hGH LCR in placental hCS, as well as pituitary hGH gene

236 nd in pituitaries of mice transgenic for the hGH locus, but not in hepatic or erythroid cells.

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

241 in pituitary somatotropes that includes the hGH LCR and adjacent CD79b locus.

242 All of the hGH cluster genes were appropriately expressed in each o

243 located -15 to -32 kilobases upstream of the hGH cluster.

244 omic insert encompassing the majority of the hGH gene cluster and the entire contiguous LCR was estab

245 ired in cis for the proper expression of the hGH gene cluster in transgenic mice.

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

248 acting through binding sites at HS-I of the hGH LCR.

249 ,II mediates long-distance activation of the hGH locus remains undefined.

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

256 Activation of the hGH transgene in the mouse is dependent on its linkage t

257 tial to full developmental activation of the hGH-N locus.

258 e employ a novel minichromosome model of the hGH-N regulatory domain and show that HSII confers robus

259 lay to levels that improved detection of the hGH-P8 fusion by almost 100-fold.

260 ely results from better accommodation of the hGH-P8 fusion protein in the phage coat.

261 Here, we demonstrate that the hGH LCR 'loops' over a distance of 28 kb in primary plac

262 Further analyses showed that the hGH minigene was expressed in several tissues, also lead

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

265 nge enhancer, HSI, located 14.5 kb 5' to the hGH promoter.

266 15 mutations within site 1 and binds to the hGH receptor (hGHR) approximately 400-fold tighter than

267 e sites (HS) HSI,II, located 15 kb 5' to the hGH-N gene.

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

270 ) located -14.5 kb to -32 kb relative to the hGH-N promoter.

271 HSII, are located 14.5 and 15.5 kb 5' to the hGH-N promoter.

272 In the regions where the hGH variant exhibits a different deuterium uptake than t

273 e former residues increase linearly with the hGH concentration in the entire concentration range beca

274 s in long-range enhancer function within the hGH locus.

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

277 creases binding affinity to sites within the hGH-LCR.

278 Among these hGH variants the distribution of the mutation is highly

279 inct sites: through its N-terminal domain to hGH, and to ECD1 through its C-terminal domain, which fo

280 the most effective ratio of Solutol HS15 to hGH was 4:1 on a mg to mg basis.

281 notype does not appear to affect response to hGH.

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).

284 Compared to wild type hGH, the variant exhibits reduced loop dynamics, indicat

285 The hGH(v)- hGH(R2) interface contains seven H-bonds, only one of wh

286 he domains of hGH(R1) that affect the hGH(v)-hGH(R2) interface indirectly.

287 , it was deleted from a previously validated hGH/P1 transgene.

288 The hGH variant (hGH(v)) contains 15 Site 1 mutations and binds>10(2) tig

289 itutive secretion and no effect on vesicular hGH stores.

290 sistent with a short-loop feedback of the VP-hGH on the endogenous GH axis.

291 The VP-hGH transgene did not affect water balance, VP storage o

292 matin modification mechanism associated with hGH LCR activity.

293 Fusion with hGH enhances the effect of a tandem dimer of thrombopoie

294 on (STAT)-3 and STAT-5 upon stimulation with hGH.

295 ly 400-fold tighter than does wild-type (wt) hGH (hGH(wt)).

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