ライフサイエンスコーパス: ACTH

1 etermination of adrenocorticotropin hormone (ACTH).

2 ocorticoids and adrenocorticotropic hormone (ACTH).

3 , cortisol, and adrenocorticotropic hormone (ACTH).

4 in response to adrenocorticotropic hormone (ACTH).

5 the release of adrenocorticotrophic hormone (ACTH).

6 mones (MSH) and adrenocorticotropin hormone (ACTH).

7 the release of adrenocorticotrophin hormone (ACTH).

8 cortisol de novo following stimulation with ACTH.

9 ant associations were found for cortisol and ACTH.

10 nd 125I-ACTH or increase cAMP in response to ACTH.

11 lower CSF levels of CRH but higher levels of ACTH.

12 illatory recruitment dynamics in response to ACTH.

13 the plasma membrane but unable to respond to ACTH.

14 ly exhibited increased lipolytic response to ACTH.

15 a membrane, where it signaled in response to ACTH.

16 essin1-A was equipotent to h/rCRF to release ACTH.

17 onse to LPS, bacterial infection, stress, or ACTH.

18 activation of PKA and lipolytic response to ACTH.

19 Neither cell type released ACTH.

20 nal markers Cyp11b1 and Cyp21 and respond to ACTH.

21 each the normal maximum cortisol response to ACTH.

22 for the 30-minute and 60-minute responses to ACTH.

23 rt showing central cardiovascular actions of ACTH.

24 (CRH) and then stimulation of the adrenal by ACTH.

25 failure to mount a steroidogenic response to ACTH.

26 -coupled receptor that mediates responses to ACTH.

27 lain reduced cortisol responses to exogenous ACTH.

28 oses >/= 30 Gy were associated with TSHD and ACTHD.

29 Microinjections (100 nl) of ACTH (0.5, 1 and 2 mmol/l) into the RVLM elicited increa

30 ng of the tripeptide LWL and the decapeptide ACTH 1-10 with amine-containing reagents.

31 d three times after intravenous cosyntropin (ACTH 1-24) injection.

32 d for some subgroups of patients, the use of ACTH (1-24) during the procedure, the most appropriate c

33 Substitution of Phe(7) with D-Phe(7) in ACTH(1-17) resulted in the loss of ligand binding and ac

34 th D-Phe or D-naphthylalanine (D-Nal(2')) in ACTH(1-24) caused a significant decrease in ligand bindi

35 Substitution of Phe(7) with D-Nal(2') in ACTH(1-24) did not switch the ligand from agonist to ant

36 us agonists alpha-MSH, beta-MSH, gamma2-MSH, ACTH(1-24), the antagonist hAGRP(87-132), and the synthe

37 r endogenous agonists alpha-MSH, gamma2-MSH, ACTH(1-24).

38 Stimulation of H295R cells with ACTH (10(-6) M) was followed by a gradual translocation

39 Corticosterone in response to intravascular ACTH (3, 10, and 250 ng/kg) 2 hrs after dexamethasone (0

40 or for chemotherapy-related adverse events (ACTH, 34% v TCH, 36.5%; P = .46).

41 e in 5-year breast cancer-specific survival (ACTH, 92% v TCH, 96%; hazard ratio, 2.08; 95% CI, 0.90 t

42 e human adrenal cortex, adrenocorticotropin (ACTH) activates CYP17 transcription by promoting the bin

43 ress axis activation, measured 2 hours after ACTH administration, involved highly specific, transient

44 of at least 5 in at least one sampling after ACTH administration.

45 n, 24 h isolation stress increased pituitary ACTH, adrenal corticosterone content and AT(1) receptor

46 monstrated the presence and functionality of ACTH, alpha- and beta-melanocyte-stimulating hormone (MS

47 nstrate H2O2-mediated oxidation of epidermal ACTH, alpha-MSH, and beta-endorphin in vitiligo owing to

48 lated cAMP, albeit with a lower potency than ACTH, alpha-MSH, and beta-MSH.

49 We show that ACTH alters pyridine nucleotide redox state and identify

50 C2R responsible for ligand selectivity using ACTH analogs and MC2R mutagenesis.

51 Some newer novel therapies such as ACTH analogues and tocilizumab require additional invest

52 thepsin L, resulted in reduced production of ACTH and accumulation of POMC.

53 We observed ACTH and alphaGSU producing cells that had prematurely d

54 pituitary AtT-20 cells resulted in increased ACTH and beta-endorphin in the regulated secretory pathw

55 ults reveal an interesting dichotomy between ACTH and cAMP with regard to regulation of CACNA1H mRNA

56 o allows properly localized receptor to bind ACTH and consequently signal.

57 duced statistically significant increases in ACTH and CORT in the participants.

58 male rats with DHT or T for 48 h reduced the ACTH and CORT response to restraint stress.

59 h lesion groups exhibiting similar levels of ACTH and corticosterone across days as the sham and no s

60 icant increase in the basal daily rhythms of ACTH and corticosterone and a significant decrease in fl

61 els in vivo, restraint stress-induced plasma ACTH and corticosterone concentrations were significantl

62 ysis, which results from decreases in plasma ACTH and corticosterone concentrations.

63 ation model have revealed large increases in ACTH and corticosterone in rats during an acute binge wi

64 Posterior BST lesions elevated plasma ACTH and corticosterone in response to acute restraint s

65 whereas TR4 knockdown decreases circulating ACTH and corticosterone levels in mice harboring ACTH-se

66 orally administered R-roscovitine suppresses ACTH and corticosterone levels, and also restrained tumo

67 orticotroph tumor growth as well as enhances ACTH and corticosterone production, whereas TR4 knockdow

68 Plasma ACTH and corticosterone recovered most rapidly after sha

69 As a consequence IL-1beta fails to evoke ACTH and corticosterone secretion in late pregnant rats,

70 ous catheters to determine concentrations of ACTH and corticosterone to assess hypothalamo-pituitary-

71 markedly attenuated the increases in plasma ACTH and corticosterone.

72 halamic microdialysate NE, as well as plasma ACTH and corticosterone.

73 e, dialysate NE and plasma concentrations of ACTH and corticosterone.

74 st prednisolone produced rapid inhibition of ACTH and cortisol pulsatility within 30 min in the morni

75 axis responses to stress, evidenced by lower ACTH and cortisol responses.

76 Prednisolone also inhibited ACTH and cortisol secretion in response to exogenous CRH

77 tropin (ACTH) secretion leading to increased ACTH and cortisol secretion throughout 24H.

78 re used to examine HPA axis activity (plasma ACTH and cortisol), immune activation (plasma IL-6), and

79 nses to social separation stress (release of ACTH and cortisol, and suppression of environmental expl

80 ress, cardiovascular activity, and levels of ACTH and cortisol, with similar responses in the 3 group

81 s drawn every 10 min for 24H and assayed for ACTH and cortisol.

82 orticosterone rhythm by both reducing plasma ACTH and differentially regulating plasma corticosterone

83 to explain the dissociated dynamics between ACTH and glucocorticoids observed under conditions of in

84 keratinocytes and skin can be stimulated by ACTH and inhibited by metyrapone (CYP11B1 enzyme inhibit

85 oopiomelanocortin (POMC) can be processed to ACTH and melanocortin peptides.

86 hrine and epinephrine levels, morning plasma ACTH and serum cortisol, fasting glucose and insulin, an

87 ermine molecular mechanisms of hMC2R binding ACTH and signaling.

88 ACTH and the metabolites may induce Ca(v)3.2 expression

89 elation, which includes early involvement of ACTH and TSH and a relatively rapid development of hypop

90 , the pituitary adrenocorticotropin hormone (ACTH) and adrenal corticosterone content, and the urinar

91 tumor-derived adrenocorticotrophic hormone (ACTH) and adrenal steroid secretion caused by pituitary

92 enocorticomelanotropic cells [corticotropin (ACTH) and alpha-melanotropin (alpha-MSH)], and with soma

93 Plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels were determined b

94 y increases the adrenocorticotropic hormone (ACTH) and corticosterone (CORT) response to stressors, a

95 Plasma adrenocorticotropic hormone (ACTH) and corticosterone levels were determined.

96 and 2.5 years, adrenocorticotropic hormone (ACTH) and cortisol concentrations were measured at basel

97 clophosphamide, paclitaxel, and trastuzumab (ACTH) and docetaxel, carboplatin, and trastuzumab (TCH).

98 se to pituitary adrenocorticotropic hormone (ACTH) and hypothalamic luteinizing hormone-releasing hor

99 treatment with adrenocorticotropic hormone (ACTH) and leukaemia inhibitory factor (LIF).

100 , stress-evoked adrenocorticotropic hormone (ACTH), and reproduction.

101 h hormone (GH), adrenocorticotropic hormone (ACTH), and thyroid stimulating hormone (TSH) in both nor

102 s of GCs on the secretion of corticotrophin (ACTH), and used molecular, genetic, and pharmacological

103 contrast, LPXRFa-R are expressed only in LH, ACTH, and alpha-MSH cells.

104 mulated plasma levels of CRH, Ucn, beta-END, ACTH, and CORT and increased skin expression of Ucn, bet

105 urocortin (Ucn), beta-endorphin (beta-END), ACTH, and corticosterone (CORT) or the brain was fixed f

106 (rapidly increased pPVN CRH mRNA expression, ACTH, and corticosterone secretion) to IL-1beta.

107 Pro-opiomelanocortin (POMC), ACTH, and cortisol were measured every 10 min from healt

108 ed triggering the successive release of CRF, ACTH, and glucocorticoids.

109 10.8% for LH/FSHD, 7.5% for TSHD, and 4% for ACTHD, and the cumulative incidence increased with follo

110 e; 2) adiponectin stimulated PRL-, inhibited ACTH- and did not alter LH/FSH/TSH-release; and 3) resis

111 regulating plasma corticosterone through an ACTH- and sympathetic nervous system-independent pathway

112 acid for the oriented immobilization of anti-ACTH antibodies onto screen-printed carbon modified elec

113 ACTH appeared to be more effective than other standard t

114 Alpha-MSH and ACTH are endogenous nonselective agonists for MC1R, MC3R

115 and gamma-melanocyte-stimulating hormone and ACTH are full agonists for all other MCRs.

116 ased adrenocortical responsiveness (cortisol:ACTH area under curve) during CRF/AVP challenge at 1.5 y

117 Fifty-five percent of infants receiving ACTH as initial treatment responded, compared to 39% for

118 eases excessive adrenocorticotropic hormone (ACTH) as a result of an adenoma arising from the ACTH-se

119 corticosterone and a consequent increase in ACTH, as expected.

120 (CORT) and the adrenocorticotropic hormone (ACTH) before and after sleep deprivation (SD) were compa

121 llele on CSF levels of CRH, plasma levels of ACTH, behavior, and ethanol consumption were assessed by

122 uitary hormones adrenocorticotropic hormone (ACTH), beta-endorphin, and alpha-melanocyte stimulating

123 nt role for cathepsin L in the production of ACTH, beta-endorphin, and alpha-MSH peptide hormones in

124 n L knock-out mice showed major decreases in ACTH, beta-endorphin, and alpha-MSH that were reduced to

125 main of MC2R resulted in a decrease in D-Phe ACTH binding affinity and potency.

126 F168 and F178 in TM4 significantly decreased ACTH binding and signaling.

127 otein (MRAP) that is absolutely required for ACTH binding and signaling.

128 n TM6, and F258 in TM7 significantly reduced ACTH-binding affinity and signaling.

129 ing undernutrition reduced pituitary output (ACTH) but increased adrenocortical responsiveness (corti

130 stimulation of adrenocorticotrophic hormone (ACTH) by hypothalamic corticotrophin-releasing hormone (

131 which activation of the adrenocorticotropin (ACTH)/cAMP signaling pathway stimulates mitochondrial tr

132 ation of Ca(v)3.2 expression in AZF cells by ACTH, cAMP analogs, and their metabolites was studied us

133 1 and to characterize the mechanism by which ACTH/cAMP regulates the biosynthesis of this molecule(s)

134 Activation of the ACTH/cAMP signal transduction cascade rapidly increases

135 Both ACTH/cAMP signaling and NADH/NAD+ ratio stimulate nuclea

136 We conclude that ACTH/cAMP stimulates PA production in the nucleus of H29

137 as response to dexamethasone suppression and ACTH challenge.

138 on Among a matched sample of older patients, ACTH compared with TCH was not associated with a higher

139 a difference in 5-year survival outcomes for ACTH compared with TCH.

140 Depressed women demonstrated increased ACTH concentrations between 4 PM and 10 PM compared to c

141 Higher plasma ACTH concentrations were associated with higher depressi

142 Pb was also associated with the ACTH:CORT ratio at baseline and throughout the course of

143 c-fos expression, together with circulating ACTH/corticosterone.

144 Adrenocorticotropic hormone (ACTH), cortisol, glucagon, and nonesterified fatty acid

145 Although ESC had no significant effects on ACTH, cortisol, IL-6, tolerance of, or adherence to IL-2

146 Differentiating a pituitary source of excess ACTH (Cushing's disease) from an ectopic source is accom

147 t adrenals with adrenocorticotropic hormone (ACTH) decreased the expression of miRNA-125a, miRNA-125b

148 ficiency, 1 had adrenocorticotropic hormone (ACTH) deficiency, and 1 had combined GH/ACTH/gonadotroph

149 ficiency due to adrenocorticotropic hormone (ACTH) deficiency.

150 44, resulting in CtBP protein partnering and ACTH-dependent CYP17 transcription.

151 Important for ACTH-dependent steroidogenesis, Mc2r, Stard1, and Cypa11

152 ex, the peptide hormone adrenocorticotropin (ACTH) directs cortisol and adrenal androgen biosynthesis

153 determined that adrenocorticotropic hormone (ACTH) enhanced FLAG-pro-GX sPLA2 processing and phosphol

154 H receptor mRNA and increased sensitivity to ACTH ex vivo.

155 It was concluded that (1) ACTH exerts excitatory effects on RVLM neurons resulting

156 in vivo showed that R-roscovitine suppresses ACTH expression, induces corticotroph tumor cell senesce

157 showed a significantly attenuated release of ACTH following 30min restraint.

158 Exposing AZF cells to ACTH for 3-6 days markedly enhanced the expression of Ca

159 ANXA1(Ac2-26)) inhibit the evoked release of ACTH from rodent anterior pituitary tissue in vitro.

160 Furthermore: 1) Leptin stimulated PRL/ACTH/FSH- but not LH/TSH-release; 2) adiponectin stimula

161 one (ACTH) deficiency, and 1 had combined GH/ACTH/gonadotrophin deficiency.

162 pin, and prolactin deficiencies, whereas for ACTH, growth hormone, and antidiuretic hormone deficienc

163 at granulosa cells and MLTC-1 cells, whereas ACTH had no effect on NHERF1 and NHERF2 mRNA levels but

164 The presence of adrenocorticotropic hormone (ACTH)-immunoreactive cells and melanocortin (MC) recepto

165 CH over time, with 88% of patients receiving ACTH in 2005 compared with 15% by 2011.

166 We suggest examining the efficacy of ACTH in preventing human osteonecrosis, a devastating co

167 etween blood and bone Pb and the increase in ACTH in response to stress.

168 a-MSH in the intermediate pituitary and with ACTH in the anterior pituitary.

169 The adrenocortical sensitivity to ACTH in the pm after CLP is suppressed progressively wit

170 Corticosterone after 10 ng/kg ACTH in the pm decreased as plasma macrophage migration

171 ed by imaging the pituitary and sampling for ACTH in the venous drainage of the pituitary.

172 on by exogenous adrenocorticotropic hormone (ACTH) in blubber of northern elephant seals due to the e

173 regression between plasma corticosterone and ACTH increased from am to pm after sham surgery (p < .05

174 ACTH increased the expression of furin and PCSK6, but no

175 data support previous studies suggesting an ACTH-independent pathway contributes to the corticostero

176 tivated hypothalamic-pituitary-adrenal axis, ACTH-independent regulators have been reported to contri

177 elanocyte-stimulating hormone (alpha-MSH) or ACTH induce ATR-pS435, enhance XPA's association with UV

178 s essential for adrenocorticotropic hormone (ACTH)-induced activation of the cAMP/protein kinase A (P

179 both basal and adrenocorticotropic hormone (ACTH)-induced stress conditions.

180 P plays a critical role in the regulation of ACTH-induced adipose lipolysis and whole-body energy bal

181 AP in 3T3-L1 adipocytes reduced or increased ACTH-induced lipolysis, respectively.

182 Specifically, ACTH induces expression of CACNA1H mRNA and Ca(v)3.2 cur

183 icroarrays in sodium-deficient mice or after ACTH infusion showed up-regulation of hypothalamic genes

184 Short tests with ACTH injection were performed on 139 patients before beg

185 Microinjection of ACTH into the RVLM increased the efferent discharge in t

186 se to exogenous adrenocorticotropic hormone (ACTH) irrespective of the plasma cortisol concentration,

187 Endogenous ACTH is the only endogenous agonist for MC2R, whereas th

188 After SD, CORT and ACTH levels have distinct patterns in WT and mPrP(0/0).

189 ACTH levels in tissue and media increased after 24h in B

190 Females had higher corticosterone and ACTH levels than males, whereas adrenal glands of MS ani

191 acement for 24 hours, and serum cortisol and ACTH levels were measured.

192 However, corticosterone levels, ACTH levels, and adrenocortical size are markedly reduce

193 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than

194 cular nucleus (PVN), and plasma cortisol and ACTH levels, were elevated only during separation in a n

195 milar results were obtained for glucagon and ACTH levels.

196 ular responses, adrenocorticotropic hormone (ACTH) levels, and cortisol levels were also measured.

197 ticosterone and adrenocorticotropin hormone (ACTH) levels.

198 ting hormones (MSH) and adrenocorticotropin (ACTH) ligands.

199 reening test but petrosal sinus sampling for ACTH may be necessary to distinguish a pituitary from an

200 d on these reports, it was hypothesized that ACTH may play a role in the regulation of cardiovascular

201 teroid resistance, all patients responded to ACTH monotherapy and ultimately achieved clinical remiss

202 he common precursor for adrenocorticotropin (ACTH) of pars distalis corticotropes and alpha-melanocyt

203 his study, we examined the role of Phe(7) in ACTH on human (h) MC1R, MC3R, and MC4R binding and signa

204 as not associated with increased circulating ACTH or a defect in the hypothalamic-pituitary axis as e

205 ents were classified as normal responders to ACTH or as abnormal responders if changes were >2 SD bel

206 fect on basal or restraint-induced levels of ACTH or corticosterone.

207 With surgical removal of ACTH or cortisol-secreting tumours, secondary adrenal in

208 to the plasma membrane but did not bind 125I-ACTH or increase cAMP in response to ACTH.

209 Data from 1,077 patients receiving ACTH or TCH were analyzed, and the propensity-matched su

210 herapy by using adrenocorticotropic hormone (ACTH) or non-steroidogenic melanocortin peptides attenua

211 d treatments of adrenocorticotropic hormone (ACTH), oral corticosteroids, and vigabatrin were conside

212 e results from enhanced secretagogue-induced ACTH output from anterior pituitary corticotrophs and ma

213 costerone (p < .001) with a modest rhythm of ACTH (p < .01) occurred only in sham rats, and the slope

214 ignificantly higher concentrations of plasma ACTH (p = 0.009).

215 as a temporal trend for increases in plasma ACTH (p=0.054); the effects of age and treatment were no

216 g multidirectional crosstalk between the CRH/ACTH pathways, autonomic nervous system, vasopressinergi

217 In this study, both truncated ACTH peptides and site-directed mutagenesis studies were

218 ufficient to respond to both small and large ACTH perturbations, but coupling this regulatory network

219 o physiological adrenocorticotropic hormone (ACTH) perturbations, ranging from basal pulses to larger

220 Our results suggest that Phe(7) in ACTH plays an important role in ligand selectivity and t

221 xpression of proopiomelanocortin (POMC), the ACTH precursor.

222 of Cushing disease (hypercortisolism due to ACTH-producing adenomas, which is the cause in approxima

223 We report that adrenocorticotropic hormone (ACTH) protects against osteonecrosis of the femoral head

224 oral fibroblasts and keratinocytes expressed ACTH receptor (MC2R), glucocorticoid receptor (GR), and

225 s demonstrated a twofold upregulation of the ACTH receptor mRNA and increased sensitivity to ACTH ex

226 The ACTH receptor, known as the melanocortin-2 receptor (MC2

227 The adrenocorticotropin (ACTH) receptor (melanocortin 2 receptor, or MC2R) is the

228 so known as the adrenocorticotropic hormone (ACTH) receptor, plays an important role in regulating an

229 ein, is required for trafficking by the MC2 (ACTH) receptor.

230 MC2 (ACTH) receptors require MC2 receptor accessory protein (

231 mimicked the inhibitory effects of ANXA1 on ACTH release as also did fMLF in high (1-100 microM) but

232 played significantly less corticosterone and ACTH release compared to sham-operated control rats only

233 rats at 1.0 mg subcutaneously, it inhibited ACTH release for >7 d.

234 te luciferase induction in HEK293T cells and ACTH release from cultured rat anterior pituitary cells.

235 XA1(1-188), ANXA1(Ac2-26), fMLF, and LXA4 on ACTH release, although at a lower concentration (50 micr

236 rimary hypothalamic neuropeptides regulating ACTH release, in the parvocellular division of paraventr

237 cortisol, but the ensuing feedback-inhibited ACTH release, when sustained for more than 1 week, has b

238 adrenaline and adrenocorticotropic hormone (ACTH) release, and arousal.

239 H/FSH/TSH-release; and 3) resistin increased ACTH-release and did not alter PRL/LH/FSH/TSH-secretion.

240 een 4 and 10 PM as well as decreased maximal ACTH response compared to control men or depressed women

241 Maximal ACTH response over time was identical between depressed

242 finasteride, for 48 h, enhanced the CORT and ACTH response to restraint stress.

243 ne self-administration (SA) desensitizes the ACTH response to self-administered nicotine but cross-se

244 the corticosterone and adrenocorticotropin (ACTH) response to immobilization stress.

245 Allopregnanolone attenuated ACTH responses to IL-1beta (500 ng/kg, i.v.) in PNS fema

246 lar habituation of plasma corticosterone and ACTH responses, heart rate, and core body temperature af

247 Organ culture studies show that ACTH-responsive cells are present at the gonad/mesonephr

248 k of the plasma adrenocorticotropic hormone (ACTH) rhythm is also reduced, the phase is dissociated f

249 nced the peak of both the corticosterone and ACTH rhythms.

250 s and increased adrenocorticotropic hormone (ACTH) secretagogue biosynthesis in the paraventricular n

251 shing disease caused by adrenocorticotropin (ACTH)-secreting pituitary adenomas leads to hypercortiso

252 Adrenocorticotropic hormone (ACTH)-secreting tumors account for 2% to 6% of adenomas

253 In ACTH-secreting and PRL-secreting adenomas, 12 and 7 gene

254 ) as a result of an adenoma arising from the ACTH-secreting cells in the anterior pituitary.

255 ACTH-secreting pituitary adenomas lead to hypercortisole

256 restrained tumor growth in a mouse model of ACTH-secreting pituitary adenomas.

257 rexpression enhanced the growth of explanted ACTH-secreting tumors and further elevated serum cortico

258 and corticosterone levels in mice harboring ACTH-secreting tumors.

259 tisol diurnal rhythm, loss of sensitivity of ACTH-secreting tumours to cortisol negative feedback, an

260 s in 44 human pituitary adenomas (25 NFAs, 7 ACTH-secreting, 7 GH-secreting, and 5 PRL-secreting aden

261 sed men demonstrated significantly decreased ACTH secretion between 4 and 10 PM as well as decreased

262 roid inhibitory effect specifically targeted ACTH secretion from pituitary corticotrophs.

263 itability and exaggerated CRH/AVP-stimulated ACTH secretion in vitro.

264 ushing's syndrome is caused either by excess ACTH secretion or by autonomous cortisol release from th

265 lying genetic basis driving tumor growth and ACTH secretion remains unsolved.

266 In mouse corticotroph EGFR transfectants, ACTH secretion was enhanced, and EGF increased Pomc prom

267 which resulted in higher Pomc expression and ACTH secretion, both of which were inhibited by gefitini

268 eptides at 100 nM; 24-72 h) increased GH and ACTH secretion, Ca(2+) and ERK1/2 signaling and cell via

269 increased proopiomelanocortin transcription, ACTH secretion, cellular proliferation, and tumor invasi

270 nal lesions and adrenocorticotropic hormone (ACTH) secretion from corticotroph or ectopic tumours hav

271 CRH) is hypothesized to drive corticotropin (ACTH) secretion leading to increased ACTH and cortisol s

272 transmembrane domain of MC2R is crucial for ACTH selectivity and potency.

273 and TM7 of hMC2R are unique and required for ACTH selectivity.

274 g with steroidogenic factor-1 in response to ACTH signaling.

275 Adrenocorticotropin (ACTH) signaling increases glucocorticoid production by p

276 Reduced adrenocortical ACTH signalling could explain reduced cortisol responses

277 on pivotally in adrenocorticotropic hormone (ACTH)-stimulated cortisol secretion.

278 ulated by NADH binding, we hypothesized that ACTH-stimulated changes in cellular pyridine nucleotide

279 icoid resulted in depression of baseline and ACTH-stimulated cortisol levels after 12 weeks of therap

280 y for preimplantation embryo development and ACTH-stimulated steroid biosynthesis.

281 that, when activated by the peptide hormone ACTH, stimulates cAMP production and adrenal steroidogen

282 their morphology and functional response to ACTH stimulation.

283 in response to adrenocorticotropin hormone (ACTH) stimulation.

284 t a short (60-minute) test with injection of ACTH (tetracosactide hexaacetate) at baseline and the da

285 Stressin1-A released slightly less ACTH than oCRF in adult adrenal-intact male rats, with i

286 Cell extracts contained significantly more ACTH than POMC, and alpha-MSH was detected only in kerat

287 ting hormones (MSH) and adrenocorticotropin (ACTH)], the antagonist agouti-related protein hAGRP(87-1

288 astic support and the stimulation of VEGF by ACTH; the latter is largely responsible for maintaining

289 lear import and adrenocorticotropic hormone (ACTH) treatment result in the dephosphorylation at the m

290 on and is unaffected by adrenocorticotropin (ACTH) treatment, loss of SUMOylation leads to enhanced S

291 ticosterone and adrenocorticotropic hormone (ACTH) under basal conditions and following restraint str

292 ata from 2005 to 2013 to compare outcomes of ACTH versus TCH among patients age older than 65 years.

293 Although ACTH was known to stimulate PKA-dependent lipolysis, the

294 At baseline, ACTH was not significantly higher (p = 0.052) in partici

295 The effects of ACTH were blocked by SHU9119 and agouti-related protein

296 The pm sham responses to all doses of ACTH were greater (p < .01) than the respective am sham

297 in the RVLM, and (3) the pressor effects of ACTH were mediated via sympathetic activation.

298 ORT) and plasma adrenocorticotropic hormone (ACTH) were assessed in response to and during recovery f

299 tained, and levels of CRH and corticotropin (ACTH) were measured by radioimmunoassay.

300 erum sample containing a certified amount of ACTH with good results.