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

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

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

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

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

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

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

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

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

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

37 ant associations were found for cortisol and ACTH.

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

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

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

41 milar results were obtained for glucagon and ACTH levels.

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

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

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

45 44, resulting in CtBP protein partnering and ACTH-dependent CYP17 transcription.

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

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

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

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

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

51 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

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

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

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

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

56 ermine molecular mechanisms of hMC2R binding ACTH and signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 lain reduced cortisol responses to exogenous ACTH.

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

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

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

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

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

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

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

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 nscriptome responses to the first and fourth ACTH administrations.

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

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

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

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

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

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

107 the release of adrenocorticotrophic hormone (ACTH).

108 the release of adrenocorticotrophin hormone (ACTH).

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

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

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

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

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

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

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

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

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

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

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

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

121 ficiency due to adrenocorticotropic hormone (ACTH) deficiency.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 ocorticoids and adrenocorticotropic hormone (ACTH).

149 , cortisol, and adrenocorticotropic hormone (ACTH).

150 in response to adrenocorticotropic hormone (ACTH).

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

152 ticosterone and adrenocorticotropin hormone (ACTH) levels.

153 in response to adrenocorticotropin hormone (ACTH) stimulation.

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

155 etermination of adrenocorticotropin hormone (ACTH).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 Plasma ACTH and corticosterone recovered most rapidly after sha

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

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

230 Higher plasma ACTH concentrations were associated with higher depressi

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

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

233 markedly attenuated the increases in plasma ACTH and corticosterone.

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

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

236 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than

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

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

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

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

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

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

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

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

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

250 Neither cell type released ACTH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 the plasma membrane but unable to respond to ACTH.

275 nal markers Cyp11b1 and Cyp21 and respond to ACTH.

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

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

278 sue to thermogenic activation in response to ACTH stimulation.

279 their morphology and functional response to ACTH stimulation.

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

281 illatory recruitment dynamics in response to ACTH.

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

283 each the normal maximum cortisol response to ACTH.

284 ly exhibited increased lipolytic response to ACTH.

285 activation of PKA and lipolytic response to ACTH.

286 failure to mount a steroidogenic response to ACTH.

287 -coupled receptor that mediates responses to ACTH.

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

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

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

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

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

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

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