ライフサイエンスコーパス: ACTH

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

2 the release of adrenocorticotrophin hormone (ACTH).

3 etermination of adrenocorticotropin hormone (ACTH).

4 ocorticoids and adrenocorticotropic hormone (ACTH).

5 , cortisol, and adrenocorticotropic hormone (ACTH).

6 in response to adrenocorticotropic hormone (ACTH).

7 the release of adrenocorticotrophic hormone (ACTH).

8 cortisol de novo following stimulation with ACTH.

9 f MC2R, a receptor for the pituitary hormone ACTH.

10 ant associations were found for cortisol and ACTH.

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

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

13 illatory recruitment dynamics in response to ACTH.

14 the plasma membrane but unable to respond 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 Neither cell type released ACTH.

19 nal markers Cyp11b1 and Cyp21 and respond to ACTH.

20 ly exhibited increased lipolytic response to ACTH.

21 activation of PKA and lipolytic response to ACTH.

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

23 failure to mount a steroidogenic response to ACTH.

24 -coupled receptor that mediates responses to ACTH.

25 lain reduced cortisol responses to exogenous ACTH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 een blubber responses to single and repeated ACTH administration, despite similarities in circulating

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

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

43 nscriptome responses to the first and fourth ACTH administrations.

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

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

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

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

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

49 gate the use of adrenocorticotropic hormone (ACTH) analogue gel in kidney transplant recipients with

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

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

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

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

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

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

56 Plasma levels of ACTH and CORT did not differ between the triple knockout

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

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

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

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

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

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

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

67 Plasma ACTH and corticosterone recovered most rapidly after sha

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

69 markedly attenuated the increases in plasma ACTH and corticosterone.

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

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

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

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

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

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

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

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

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

79 ly expressed (DEGs) in response to the first ACTH and fourth administrations, respectively, 24 DEGs b

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

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

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

83 d statistically significant decrease in PRL, ACTH and non-functional subtypes when compared to LH/FSH

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

85 ermine molecular mechanisms of hMC2R binding ACTH and signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 10.8% for LH/FSHD, 7.5% for TSHD, and 4% for ACTHD, and the cumulative incidence increased with follo

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

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

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

111 ACTH appeared to be more effective than other standard t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 1 and to characterize the mechanism by which ACTH/cAMP regulates the biosynthesis of this molecule(s)

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

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

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

135 us monkey acute adrenocorticotropic hormone (ACTH) challenge model and demonstrated a superior 100-fo

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

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

138 Higher plasma ACTH concentrations were associated with higher depressi

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

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

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

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

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

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

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

146 ficiency due to adrenocorticotropic hormone (ACTH) deficiency.

147 44, resulting in CtBP protein partnering and ACTH-dependent CYP17 transcription.

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

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

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

151 ls of oxytocin, adrenocorticotropic hormone (ACTH), estradiol, progesterone and testosterone.

152 ohorts showed elevated basal oxytocin, lower ACTH, estradiol, progesterone and testosterone compared

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

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

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

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

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

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

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

160 ACTH gel to 3.3 +/- 2.3 g/g after the use of ACTH gel (P = 0.004).

161 h, the response varied among the recipients, ACTH gel might be an effective therapy for posttransplan

162 from a mean +/- SD of 8.6 +/- 7.6 g/g before ACTH gel to 3.3 +/- 2.3 g/g after the use of ACTH gel (P

163 tuximab, which was started before the use of ACTH gel.

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

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

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

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

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

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

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

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

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

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

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

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

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

177 /GCF protein concentrations was detected for ACTH (increased in GG only) and insulin, leptin, osteoca

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than

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

197 milar results were obtained for glucagon and ACTH levels.

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

199 ticosterone and adrenocorticotropin hormone (ACTH) levels.

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

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

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

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

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

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

206 we administered adrenocorticotropic hormone (ACTH) once daily for four days to free-ranging juvenile

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 fourth pre-ACTH samples, and 12 DEGs between ACTH response samples from the first and fourth days.

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

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

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

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

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

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 ly, 24 DEGs between the first and fourth pre-ACTH samples, and 12 DEGs between ACTH response samples

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

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

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

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

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

256 ACTH-secreting pituitary adenomas lead to hypercortisole

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

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

259 When compared with LH/FSH-secreting tumors, ACTH-secreting tumors showed statistically significant d

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

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

262 mas (PRL-secreting) = 11, Cushing's disease (ACTH-secreting) = 4, non-functional = 5, and mixed = 8]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 Adrenocorticotropin (ACTH) signaling increases glucocorticoid production by p

278 Reduced adrenocortical ACTH signalling could explain reduced cortisol responses

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

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

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

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

283 sue to thermogenic activation in response to ACTH stimulation.

284 their morphology and functional response to ACTH stimulation.

285 in response to adrenocorticotropin hormone (ACTH) stimulation.

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

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

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

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

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

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

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.