ライフサイエンスコーパス: ACTH

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

2 ACTH appeared to be more effective than other standard t

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

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

5 ACTH-secreting pituitary adenomas lead to hypercortisole

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

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

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

9 Reduced adrenocortical ACTH signalling could explain reduced cortisol responses

10 Adrenocorticotropin (ACTH) signaling increases glucocorticoid production by p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 gnificantly decreased the corticosterone and ACTH response to immobilization.

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

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

37 stress induced release of corticosterone and ACTH.

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

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

40 ant associations were found for cortisol and ACTH.

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

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

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

44 milar results were obtained for glucagon and ACTH levels.

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

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

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

48 44, resulting in CtBP protein partnering and ACTH-dependent CYP17 transcription.

49 as response to dexamethasone suppression and ACTH challenge.

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

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

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

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

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

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

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

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

58 ermine molecular mechanisms of hMC2R binding ACTH and signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 lain reduced cortisol responses to exogenous ACTH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 the release of adrenocorticotrophic hormone (ACTH).

106 the release of adrenocorticotrophin hormone (ACTH).

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

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

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

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

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

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

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

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

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

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

117 ficiency due to adrenocorticotropic hormone (ACTH) deficiency.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 ocorticoids and adrenocorticotropic hormone (ACTH).

144 , cortisol, and adrenocorticotropic hormone (ACTH).

145 in response to adrenocorticotropic hormone (ACTH).

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

147 ticosterone and adrenocorticotropin hormone (ACTH) levels.

148 in response to adrenocorticotropin hormone (ACTH) stimulation.

149 etermination of adrenocorticotropin hormone (ACTH).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 Maximal ACTH response over time was identical between depressed

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

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

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

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

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

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

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

187 rt showing central cardiovascular actions of ACTH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Plasma ACTH and corticosterone recovered most rapidly after sha

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

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

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

232 Higher plasma ACTH concentrations were associated with higher depressi

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

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

235 markedly attenuated the increases in plasma ACTH and corticosterone.

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

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

238 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than

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

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

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

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

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

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

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

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

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

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

249 Neither cell type released ACTH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 the plasma membrane but unable to respond to ACTH.

274 nal markers Cyp11b1 and Cyp21 and respond to ACTH.

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

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

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

278 their morphology and functional response to ACTH stimulation.

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

280 illatory recruitment dynamics in response to ACTH.

281 ly exhibited increased lipolytic response to ACTH.

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

283 activation of PKA and lipolytic response to ACTH.

284 each the normal maximum cortisol response to ACTH.

285 failure to mount a steroidogenic response to ACTH.

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

287 -coupled receptor that mediates responses to ACTH.

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

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

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

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

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

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

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

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

296 1 and to characterize the mechanism by which ACTH/cAMP regulates the biosynthesis of this molecule(s)

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

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

299 cortisol de novo following stimulation with ACTH.

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