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1 being nuclear RNA enriched and regulated by growth hormone.
2 tion of oleic acid and the overproduction of growth hormone.
3 ed Down syndrome, vitamin A derivatives, and growth hormone.
4 an RNA methyltransferase, and GH1, encoding growth hormone.
5 t be rescued by administration of ghrelin or growth hormone.
6 UAG, reduced DI and kg and increased plasma growth hormone.
7 -onset gigantism resulting from an excess of growth hormone.
8 clamps, increased plasma corticosterone and growth hormone.
9 sometimes associated with hypersecretion of growth hormone.
10 s for the mammatrophic hormones estrogen and growth hormone.
11 position, which may affect the regulation of growth hormones.
12 pond to inflammatory cytokines, insulin, and growth hormones.
17 and IL-22, and hormonal modulation including growth hormone administration and sex steroid inhibition
19 b, letrozole, Y-27632, octreotide, and human growth hormone, all delivered at clinically-relevant dos
22 s a G-protein-coupled receptor that controls growth hormone and insulin secretion, food intake, and r
23 sregulation of gene networks associated with growth hormone and insulin signaling, including inductio
26 ole for MIR205HG as an lncRNA that regulates growth hormone and prolactin production in the anterior
27 at GH3 cells, it led to increased release of growth hormone and proliferation of growth hormone-produ
28 gly, this period of growth is independent of growth hormone and the underlying mechanism is poorly un
29 aly is characterized by increased release of growth hormone and, consequently, insulin-like growth fa
30 od for the bacteria and the bacteria produce growth hormones and antibiotics for the algae, or parasi
31 red in the presence or the absence of IGF-1, growth hormone, and an IGF-1 receptor-blocking antibody.
32 nd prolactin deficiencies, whereas for ACTH, growth hormone, and antidiuretic hormone deficiency dyna
36 ma concentrations of 25 different cytokines, growth hormones, and other factors which have previously
40 roduction of insulin-like growth factor 1 or growth hormone, are involved in the pathogenesis of gluc
41 -microglobulin, immunoglobulin G1, and human growth hormone as model systems, we demonstrate that DEP
42 of ghrelin, which includes the secretion of growth hormone, as well as the stimulation of appetite,
44 leads to the formation of a gradient of the growth hormone auxin across the photo-stimulated stem.
47 e directional, cell-to-cell transport of the growth hormone auxin to generate an asymmetric auxin res
48 ating glucose, altered lipid metabolism, and growth hormone axis perturbations, can promote senescent
49 ich may relate to contamination of different growth hormone batches with different strains of human p
50 onstrated functional complexation with human growth hormone binding protein (hGHBp) to the different
51 bances (leptin, afamin), stunting of growth (growth hormone binding protein), and connective tissue r
53 e inadequately controlled (5-point, 2 h mean growth hormone concentration >2.5 mug/L and insulin-like
54 hieving biochemical control, defined as mean growth hormone concentration less than 2.5 mug/L and nor
55 ous treatment (octreotide or lanreotide) and growth hormone concentrations at screening (2.5-10 mug/L
56 tion in childhood has been related to higher growth-hormone concentrations that may affect mammary gl
59 ns of epinephrine, norepinephrine, glucagon, growth hormone, cortisol, endogenous glucose production,
62 The most common endocrine disorders were growth hormone deficiency (12.5%), precocious puberty (1
64 yroid cancer (HR, 9.2; 95% CI, 6.2 to 13.7), growth hormone deficiency (HR, 5.3; 95% CI, 4.3 to 6.4),
66 h whole-genome resequencing in patients with growth hormone deficiency and maternally inherited gingi
67 crinology clinic where he was diagnosed with growth hormone deficiency and was started on replacement
68 he regulation of human growth, and show that growth hormone deficiency associated with maternally inh
70 treatment on fracture risk in patients with growth hormone deficiency from the international Hypopit
72 ocus, in a large family in which an isolated growth hormone deficiency segregates as an autosomal dom
73 this prospective cohort study, patients with growth hormone deficiency were analysed from the HypoCCS
74 ive against fracture for adult patients with growth hormone deficiency without previously reported os
75 with adrenocorticotropic hormone deficiency, growth hormone deficiency, and mild ectodermal dysplasia
76 or older and had an established diagnosis of growth hormone deficiency, either alone or with multiple
78 syndrome, coeliac disease, cystic fibrosis, growth hormone deficiency, renal tubular acidosis, and s
81 ynthesis and secretion of VLDL-TAG using the growth hormone-deficient Ames dwarf mouse model, which h
84 rns with muscularity and use of supplements, growth hormone derivatives, or anabolic steroids to achi
85 t source of infecting prion contamination of growth hormone derived from a patient with Creutzfeldt-J
87 ase due to administration of cadaver-sourced growth hormone during childhood are still being seen in
89 erentiated further into cholangiocytes using growth hormone, epidermal growth factor, interleukin-6,
90 xposure of young and old HSCs to recombinant growth hormone ex vivo led to diminished short-term reco
91 ta after systemic injections of contaminated growth hormone extracts or dura mater grafts derived fro
93 date genes in these two regions included the growth hormone gene (GH1) on SSC12 and PRKD1 on SSC7.
97 he transmembrane domains of the receptors of growth hormone (GH) and insulin-like growth factor 1 (IG
101 Both pathological excess and deficiency of growth hormone (GH) are associated with cardiovascular m
103 ats with monosodium glutamate (MSG), a total growth hormone (GH) blocker, and, using cultured hepatoc
111 somatotroph adenomas result in dysregulated growth hormone (GH) hypersecretion and acromegaly; howev
112 om mice that overexpress or are deficient in growth hormone (GH) indicate that GH stimulates T and B-
115 e potential dysfunction caused by changes in growth hormone (GH) levels after brain death (BD), and t
117 ver disease (NAFLD) are reported to have low growth hormone (GH) production and/or hepatic GH resista
119 dies have shown that PVH neurons express the growth hormone (GH) receptor (GHR), although the role of
120 Ghrelin is a peptide hormone that stimulates growth hormone (GH) release and positive energy balance
124 cate until now that the pulsatile pattern of growth hormone (GH) secretion is primarily controlled by
125 s is shaped by the male pattern of pituitary growth hormone (GH) secretion that determines body size
126 a close relationship between food intake and growth hormone (GH) secretion; however, the mechanism th
129 s have underscored the importance of hepatic growth hormone (GH) signaling in the development of NAFL
132 ytokine signaling 2 (SOCS2), an inhibitor of growth hormone (GH) signaling, was strongly induced afte
133 transcription factor STAT5 in liver impairs growth hormone (GH) signalling and thereby promotes fatt
134 study investigates the efficacy of systemic growth hormone (GH) therapy in ameliorating the deleteri
135 expression is transcriptionally regulated by growth hormone (GH) through growth hormone response elem
137 f iatrogenic Creutzfeldt-Jakob disease after growth hormone (GH) treatment provide an opportunity to
138 We also examined links between ghrelin and growth hormone (GH), a major downstream effector of the
141 pituitary hormones such as prolactin (PRL), growth hormone (GH), adrenocorticotropic hormone (ACTH),
142 ising minimum cortisol and high aldosterone, growth hormone (GH), and prolactin levels, thereby presu
143 Pediatric patients have been treated with growth hormone (GH), and recent findings suggest that bl
144 ncentration of circulating hormones, such as growth hormone (GH), but the biological functions of thi
145 Growth hormone-releasing hormone (GHRH) and Growth hormone (GH), underappreciated findings in ARID1B
146 n is mediated by a marked increase in plasma growth hormone (GH), which is elicited by an increase in
147 ggest that loss of MC4R function may enhance growth hormone (GH)-mediated growth, although this remai
149 BA; 20 ppm in feed) or Reporcin (recombinant growth hormone; GH; 10 mg/48 hours injected) and compare
150 on, and activity levels) and deficiencies in growth hormone (GHD) and/or sex steroids with low BMD an
153 eric dynamics by conducting studies on human growth hormone (hGH) and pyrin domain (PYD), and the res
154 and tissue-specific activation of the human growth hormone (hGH) gene cluster in the pituitary and p
159 , we contrast IgG binding with that of human growth hormone (hGH) to its receptor (hGH-R) which displ
162 estigated the weak self-association of human growth hormone (hGH, KD = 0.90 +/- 0.03 mM) at neutral p
163 leaf closure has been associated with plant growth hormones, how mechanical forces actuate the proce
165 Mechanistically, direct upregulation of the growth hormone IGF2 emerged as a mediator of the aggress
166 previously unrecognized role for ghrelin and growth hormone in maladaptive changes following prolonge
168 findings demonstrate the functional role of growth hormone in promoting thrombopoiesis and provide a
169 characterizing the interaction between human growth hormone in solution and the corresponding antibod
170 n (adrenocorticotropic hormone, cortisol and growth hormone) increased in spring in both strains but
171 nitial step in the biosynthesis of the plant growth hormone indole-acetic acid by bacterial pathogens
172 Igf-1 transcription is regulated through growth hormone-induced, JAK2 kinase-mediated phosphoryla
173 which carry single-gene mutations within the growth-hormone, insulin/IGF-1 or mTOR signalling pathway
174 e mice promotes growth while suppressing the growth hormone-insulin-like growth factor-1 (GH-IGF-1) a
175 oduction and associates with abrogation of a growth hormone/insulin-like growth factor 1 (GH/IGF1) ax
176 As IGFBP3 plays a key role in regulating the growth hormone/insulin-like growth factor type 1 (GH/IGF
181 crosis factor-alpha, cortisol, glucagon, and growth hormone levels increased, and free fatty acids an
183 ated insulin-like growth factor 1 levels and growth hormone levels; initial treatment is surgical.
184 ed important biological functions related to growth, hormone levels affecting female fertility, physi
186 study was to test whether fasting levels of growth hormone measured with a high-sensitivity assay (h
187 escent host liver repopulation involving the growth hormone-mediated release of the transcriptional b
189 nile than in senescent rats, suggesting that growth hormone might promote host liver repopulation.
192 ne disease, and the use of recombinant human growth hormone provide some hope for catch-up growth in
197 rtial hepatectomy by preventing increases in growth hormone receptor (GHR) via ubiquitination, suppre
198 lication FDR-corrected p = 2.18 x 10-2), and growth hormone receptor (GHR, Discovery FDR-corrected p
199 with phosphorylated peptides from substrates growth hormone receptor (GHR-pY595) and erythropoietin r
203 .SIGNIFICANCE STATEMENT People and mice with growth hormone receptor deficiency (GHRD or Laron syndro
206 ncident type 2 diabetes were aminoacylase-1, growth hormone receptor, and insulin-like growth factor-
208 ons, as well as sex-biased binding sites for growth hormone-regulated transcriptional activators (STA
209 including two rat lincRNAs showing the same growth hormone-regulated, sex-biased expression as their
210 for five transcription factors implicated in growth hormone-regulated, sex-biased liver gene expressi
211 states, transcription factor occupancy, and growth hormone regulation provides novel insights into t
212 ghrelin, responsible for the stimulation of growth hormone release and appetite, little is known of
216 uteinizing hormone releasing hormone (LHRH), growth hormone releasing hexapeptide (GHRP-6), and TrpCa
217 elanocortin (POMC), neuropeptide Y (NPY) and growth hormone releasing hormone (GHRH) neurons, regulat
218 s LHn from serotype D with a fragment of the growth hormone releasing hormone, has previously reveale
221 ) deficiency with inadequate compensation by Growth hormone-releasing hormone (GHRH) and Growth hormo
222 therapeutic effects of agonistic analogs of growth hormone-releasing hormone (GHRH) and their mechan
226 eurons, and two growth-stimulatory peptides, growth hormone-releasing hormone (GHRH) for GHRH-neurons
232 ith corticotropin-releasing factor (CRF) and growth hormone-releasing hormone (GHRH), suggesting nove
236 re transplantation using a potent agonist of growth-hormone-releasing hormone (GHRH) to promote islet
237 ntrolled studies of the effects of long-term growth hormone replacement on fracture risk in adult pat
239 es chronic systemic inflammation, leading to growth hormone resistance and impaired linear growth.
240 alamic amenorrhoea; a nutritionally acquired growth-hormone resistance leading to low concentrations
241 pmental maturation of hepatic IGF-1 intron 2 growth hormone response element (IN2GHRE) histone methyl
242 stal weak enhancer (IGF-1 5'-upstream region growth hormone response element; 5URGHRE) as a GHRE spec
244 ine, norepinephrine, glucagon, cortisol, and growth hormone responses were similarly reduced after al
249 for the quantification of recombinant human growth hormone (rhGH) in serum has been developed using
251 g periods and acts through its receptor, the growth hormone secretagogue 1a (GHSR1a), to promote food
252 ained another unapproved drug, including the growth hormone secretagogue ibutamoren, the peroxisome p
253 The truncated non-signaling ghrelin receptor growth hormone secretagogue R1b (GHS-R1b) has been sugge
254 Ghrelin's effect is mediated by its receptor Growth Hormone Secretagogue Receptor (GHS-R), but the ph
255 y format designed for the early detection of growth hormone secretagogue receptor (GHS-R1a) antagonis
259 ells produce ghrelin and delta-cells express growth hormone secretagogue receptor (GHSR), suggesting
261 actions of ghrelin are mediated through the growth hormone secretagogue receptor 1a (ghrelin recepto
263 by the stomach and acts at its receptor, the growth hormone secretagogue receptor 1a (GHSR1a), in the
264 n-KO mice and C57BL/6N mice administered the growth hormone secretagogue receptor agonist HM01 or veh
265 modeling, we demonstrate that binding to the growth hormone secretagogue receptor is accompanied by a
266 ility by activating KATP conductance via the growth hormone secretagogue receptor subtype 1a-Galphai
268 tion of a postsynaptic ghrelin receptor, the growth hormone secretagogue receptor type 1a (GHS-R1a),
271 ly by the expression of the ghrelin receptor growth hormone secretagogue type 1a (GHS-R1a) in the hyp
274 ge repair pathways were affected by SCNAs in growth hormone-secreting (GH-secreting) somatotroph aden
275 IP) mutation-induced aggressive, young-onset growth hormone-secreting pituitary tumors are not fully
277 otropic effects including the stimulation of growth hormone secretion and subsequent increase of insu
278 ed receptor GHS-R1a mediates ghrelin-induced growth hormone secretion, food intake, and reward-seekin
279 number of physiological processes including growth hormone secretion, food intake, as well as energy
281 /-) mice had increased activation of hepatic growth hormone-signal transducer and activator of transc
282 mportant for GI health, nutrient harvest and growth hormone signaling, including decreased abundance
283 ed on the responses of the liver lincRNAs to growth hormone stimulation, which imparts clinically rel
285 ence rate was lower in patients who received growth hormone than in those who did not (fracture incid
289 Deciding when to pursue recombinant human growth hormone therapy to increase adult height is contr
290 ntiepileptic drugs and the efficacy of human growth hormone therapy, and few data are available for t
293 between patients who did and did not receive growth hormone treatment in the subgroup of patients wit
299 epends on the action of the gibberellin (GA) growth hormones, which promote cell production in the ro
300 e expression of Pit1, Zbtb20, prolactin, and growth hormone, while its overexpression enhanced the le