ライフサイエンスコーパス: steroidogenesis

1 ion, SR-BI-mediated selective CE uptake, and steroidogenesis.

2 ipotency, lipid and glucose homeostasis, and steroidogenesis.

3 arian regulators of follicle development and steroidogenesis.

4 R-BI expression, selective CE transport, and steroidogenesis.

5 us, facilitates cholesterol availability for steroidogenesis.

6 an unfolded state, unable to induce maximal steroidogenesis.

7 n (HDL) cholesteryl ester (CE) transport and steroidogenesis.

8 gamma expression potentiates hormone-induced steroidogenesis.

9 omal recessive metabolic disorder of adrenal steroidogenesis.

10 y AR antagonism in addition to inhibition of steroidogenesis.

11 ate-induced suppression of fetal Leydig cell steroidogenesis.

12 ia, which is the site of the initial step in steroidogenesis.

13 nografts, but only rats exhibited suppressed steroidogenesis.

14 1), suggesting a regulatory role of HIF-1 in steroidogenesis.

15 e of leptin in hypoxia-induced disruption of steroidogenesis.

16 important regulatory signals for control of steroidogenesis.

17 representing a new role for translocases in steroidogenesis.

18 -1) is essential for adrenal development and steroidogenesis.

19 Plasma membrane cholesterol trafficking in steroidogenesis.

20 biophysical properties that imply a role in steroidogenesis.

21 at the reptilian brain is capable of de novo steroidogenesis.

22 alyzes the initial and rate-limiting step of steroidogenesis.

23 ies are distinct from its activity to induce steroidogenesis.

24 ACTH, stimulates cAMP production and adrenal steroidogenesis.

25 it is converted to pregnenolone to initiate steroidogenesis.

26 aining adrenocortical function, specifically steroidogenesis.

27 PDE8A is a key regulator of LH signaling and steroidogenesis.

28 KA, inhibited both basal and hormone-induced steroidogenesis.

29 vesicular trafficking of PM cholesterol for steroidogenesis.

30 s on mitochondrial cholesterol transport and steroidogenesis.

31 ase in cholesterol efflux and an increase in steroidogenesis.

32 tary pool of cAMP that mediates LH-regulated steroidogenesis.

33 sion of key regulators of gonadal growth and steroidogenesis.

34 rol is converted to pregnenolone, initiating steroidogenesis.

35 les in the control of spermatogenesis and/or steroidogenesis.

36 embrane and is a critical regulatory step in steroidogenesis.

37 ment from lipid droplets to mitochondria for steroidogenesis.

38 ons such as the detection of gross errors in steroidogenesis.

39 trus phase of the estrous cycle and aberrant steroidogenesis.

40 alpha-SNAP in Y1 cells decreased stimulated steroidogenesis.

41 steroid hydroxylase genes, key mediators of steroidogenesis.

42 a conserved role in gonadal development and steroidogenesis.

43 insulin sensitivity or to direct effects on steroidogenesis.

44 ), which depletes glutathione and stimulates steroidogenesis.

45 n (StAR) determines adrenal and gonadal cell steroidogenesis.

46 so its selective modulation of FSH action in steroidogenesis.

47 omegestone and to inhibit the hCG-stimulated steroidogenesis.

48 sis and the 22R-hydroxycholesterol-supported steroidogenesis.

49 By contrast, BMP-15 alone had no effect on steroidogenesis.

50 e involvement of the lipoxygenase pathway in steroidogenesis.

51 , we examined PM cholesterol trafficking for steroidogenesis.

52 nship between AA and cAMP in hormone-induced steroidogenesis.

53 or Kit in Leydig cell differentiation and/or steroidogenesis.

54 are required for trophic hormone-stimulated steroidogenesis.

55 eceptors, plays an important role in gonadal steroidogenesis.

56 ertoire of SF-1-responsive genes involved in steroidogenesis.

57 avage enzyme gene, and consequently, promote steroidogenesis.

58 a-SNAP restored, the PMs' ability to support steroidogenesis.

59 zyme carries out the first committed step in steroidogenesis.

60 vivo showed features associated with active steroidogenesis.

61 mutations was observed on the stimulation of steroidogenesis.

62 ssential roles in adrenocortical and gonadal steroidogenesis.

63 s lacking the protein retained low levels of steroidogenesis.

64 otein is coordinately regulated with adrenal steroidogenesis.

65 d enhance ROS production, leading to reduced steroidogenesis.

66 h severe skeletal deformities and disordered steroidogenesis.

67 confirming the requirement of SCAP-SREBP2 in steroidogenesis.

68 ckout approaches to test the role of SCAP in steroidogenesis.

69 REBP activation and subsequent regulation of steroidogenesis.

70 hich are postulated to provide substrate for steroidogenesis.

71 acids may affect prostaglandin synthesis and steroidogenesis.

72 lular levels of cholesterol, a substrate for steroidogenesis.

73 entral location for initiating mitochondrial steroidogenesis.

74 of a blockade of cholesterol utilization for steroidogenesis.

75 or agonists nor did they cause reductions in steroidogenesis.

76 l adrenal hyperplasia, a disorder of adrenal steroidogenesis.

77 itates the rate-limiting step of aldosterone steroidogenesis.

78 multiple key reactions at the heart of human steroidogenesis.

79 lure to accumulate lipid droplets needed for steroidogenesis.

80 an steroidogenic cell lines had no effect on steroidogenesis.

81 asis for these defects appears to be altered steroidogenesis, a direct result of the lack of HDL-C.

82 ity, POR missense mutations cause disordered steroidogenesis, ambiguous genitalia, and Antley-Bixler

83 nduced allergic responses through effects on steroidogenesis, an essential pathway in T(H)2 different

84 sed for intracellular protein expression and steroidogenesis analyses, respectively.

85 s reveal novel functions of SRA and Dax-1 in steroidogenesis and adrenal biology.

86 t and levoketoconazole are new inhibitors of steroidogenesis and are currently being evaluated in mul

87 p53-dependent apoptosis and is necessary for steroidogenesis and biogenesis of iron-sulfur clusters.

88 ntifungal azole ketoconazole interferes with steroidogenesis and can cause adrenal insufficiency, flu

89 several cancer cells where it is involved in steroidogenesis and cell proliferation, respectively.

90 tudy has revealed an altered Smad signaling, steroidogenesis and cell viability upon modulation of BM

91 Steroidogenesis and cell viability were studied to explo

92 controlling the P450 enzymes, which regulate steroidogenesis and cranial bone formation.

93 entified 1,906 genes with potential roles in steroidogenesis and developmental timing.

94 similarly by FSH and PKA-CQR are involved in steroidogenesis and differentiation, while transcripts m

95 To examine the definitive role of TSPO in steroidogenesis and embryo development, we generated glo

96 amined the ability of the mutants to promote steroidogenesis and enter the mitochondria of transfecte

97 are adequate for maintenance of Leydig cell steroidogenesis and fertility because of partial functio

98 n (StAR) is required for adrenal and gonadal steroidogenesis and for male sexual differentiation.

99 ormone (FSH) act on gonadal cells to promote steroidogenesis and gametogenesis.

100 te their development and functions including steroidogenesis and gametogenesis.

101 key role for apoE in the tonic inhibition of steroidogenesis and HPA axis activity and have important

102 17A1 is an enzyme that plays a major role in steroidogenesis and is critically involved in the biosyn

103 amily, plays a key role in the regulation of steroidogenesis and is expressed at high levels in stero

104 A pathway-guided analysis revealed ovarian steroidogenesis and leptin signaling as highly relevant

105 We found that PTTH concomitantly promotes steroidogenesis and light avoidance at the end of larval

106 , although the Gipr is essential for adrenal steroidogenesis and links HF feeding to increased levels

107 ved that exogenous RFRP-3 suppresses gonadal steroidogenesis and mating behavior in NMRs given the op

108 remains unclear because its presumed role in steroidogenesis and mitochondrial permeability transitio

109 vidence for the role of miRNAs in regulating steroidogenesis and novel insights into the molecular me

110 expression patterns of genes involved in sex steroidogenesis and processing.

111 ted safety, pharmacokinetics, and effects on steroidogenesis and prostate-specific antigen (PSA) leve

112 t to show the in vivo requirements of SF1 in steroidogenesis and provides novel data on the cellular

113 need to enter into mitochondria to stimulate steroidogenesis and that residues in the C terminus are

114 helicase could be relevant to the control of steroidogenesis and the paracrine regulation of androgen

115 ription factors may have a role in cutaneous steroidogenesis and thus be involved in hair follicle cy

116 a range of biochemical processes, including steroidogenesis and vitamin D metabolism.

117 Focusing on ovarian steroidogenesis and vitellogenin uptake, we depict the m

118 ailability of cholesterol, the substrate for steroidogenesis), and a failure to mount a steroidogenic

119 oteins associated with steroid transport and steroidogenesis, and androgen levels were restored in mu

120 ng the regulation of cholesterol metabolism, steroidogenesis, and apoptosis.

121 es coordinately regulate its expression with steroidogenesis, and in the liver, where it may particip

122 of other cytochrome P450 enzymes involved in steroidogenesis, and interference can pose a liability i

123 e a structural basis for understanding human steroidogenesis, and pave the way for the design of more

124 nt pathways, cGMP signaling also can promote steroidogenesis, and PDE5 modulates this process.

125 the intracellular messenger for LH action on steroidogenesis, and pharmacological evidence indicates

126 ese results suggest that mVL30 RNA regulates steroidogenesis, and possibly other physiological proces

127 ne factors, extracellular matrix components, steroidogenesis, and prolactin dynamics.

128 Therefore, Tom22 is a critical regulator of steroidogenesis, and thus, it is essential for mammalian

129 s of CMKLR1 signaling in DHT-induced ovarian steroidogenesis, antral follicles were isolated from wil

130 involved in various cell functions including steroidogenesis, apoptosis, and proliferation.

131 Vitamin E transport and steroidogenesis are closely associated with low-density

132 he regulation of ovarian follicle growth and steroidogenesis are now established, noncanonical WNT si

133 etic defects in adrenal gland development or steroidogenesis) are not born with respiratory insuffici

134 s, such as detoxification of xenobiotics and steroidogenesis, are based on the ability to catalyse th

135 This study demonstrates T cell de novo steroidogenesis as a mechanism of anti-tumor immunosuppr

136 late mixture directly affected expression of steroidogenesis as demonstrated in a relevant in vitro m

137 tion of steroid hormones by use of the H295R steroidogenesis assay, and sex steroid receptor binding

138 showed StAR-like activity in a cell culture steroidogenesis assay, indicating cholesterol transfer.

139 calcin also governed adrenal growth, adrenal steroidogenesis, blood pressure, electrolyte equilibrium

140 tor therapy to be an effective stimulator of steroidogenesis, both PDE8 isozymes and PDE4 need to be

141 nce (MIS) is implicated in the regulation of steroidogenesis, breast and prostate growth, and ovarian

142 ues, where it is coordinately regulated with steroidogenesis by adrenocorticotropic hormone (ACTH), h

143 strate cholesterol into the mitochondria for steroidogenesis by an unknown mechanism.

144 strate that 14-3-3gamma negatively regulates steroidogenesis by binding to Ser-194 of STAR, thus keep

145 et of conformations likely to modulate human steroidogenesis by CYP17A1, demonstrating that this appr

146 d transiently functions at the initiation of steroidogenesis by delaying maximal steroidogenesis in M

147 tory protein (StAR) plays a critical role in steroidogenesis by enhancing the delivery of substrate c

148 tentiates adrenocorticotropin stimulation of steroidogenesis by increasing cAMP-dependent protein kin

149 rotein (StAR) stimulates adrenal and gonadal steroidogenesis by increasing the influx of cholesterol

150 nt mutant StAR protein that cannot stimulate steroidogenesis by isolated mitochondria did not promote

151 low cAMP levels, thereby suppressing resting steroidogenesis by keeping CEH/HSL inactive and StAR pro

152 StAR (StARD1) induces adrenal and gonadal steroidogenesis by moving cholesterol from the outer mit

153 cceptor mitochondrial membranes and enhanced steroidogenesis by placental mitochondria.

154 ole of the CRAC domain of PBR in Leydig cell steroidogenesis by using a transducible peptide composed

155 We tested the ability of MLN64 to stimulate steroidogenesis by using COS-1 cells cotransfected with

156 We conclude that MLN64 stimulates steroidogenesis by virtue of its homology to StAR.

157 downstream gene products is required before steroidogenesis can occur.

158 P450 17A1 has a major role in steroidogenesis, catalyzing the two-step oxidations of p

159 ) enzyme operates at a key juncture of human steroidogenesis, controlling the levels of mineralocorti

160 inase and serine proteinase inhibitors), and steroidogenesis (CYP21A2 and progesterone receptor).

161 on is dependent upon SF-1, cAMP induction of steroidogenesis does not enhance the responsiveness of a

162 (CYP17A1), a rate-limiting enzyme in adrenal steroidogenesis, does not inhibit bacterial desmolase (D

163 Pharmacological inhibition of steroidogenesis during development blocked the productio

164 These results reveal genes regulating steroidogenesis during development that likely modulate

165 ogesterone production in a way that reflects steroidogenesis during the normal estrous cycle.

166 hyperplasia is a family of inborn errors of steroidogenesis, each characterized by a specific enzyme

167 al of N-terminal sequences increased MLN64's steroidogenesis-enhancing activity.

168 residues in the C terminus are essential for steroidogenesis-enhancing activity.

169 terminus (N-62) did not significantly affect steroidogenesis-enhancing activity.

170 d steroid synthesis, suggesting HSL-mediated steroidogenesis entails enhanced oxysterol production.

171 In vertebrates, the steroidogenesis enzyme 5alpha-reductase converts testost

172 ed alterations in steroid hormone receptors, steroidogenesis enzymes, and specifically, the circadian

173 significant species-specific differences in steroidogenesis, especially CYP17A1 expression and activ

174 We show that, in 4-month-old PACAP-/- mice, steroidogenesis (evaluated by levels of testosterone, st

175 iofacial dysmorphogenesis, and/or disordered steroidogenesis, exhibiting ambiguous genitalia.

176 ry protein (StAR) plays an essential role in steroidogenesis, facilitating delivery of cholesterol to

177 -activated receptor gamma coactivator-1alpha/steroidogenesis factor-1-dependent upregulation of aldos

178 ryo development and led to the alteration of steroidogenesis gene transcripts at nanogram per liter c

179 osis genes and with diminished expression of steroidogenesis genes Star, Cyp11a1, and Hsd3b1.

180 in vivo role of this transcription factor in steroidogenesis has not been elucidated.

181 Its role in cAMP-mediated control of steroidogenesis has not been explored.

182 f GRTH associated with gonadotropin-mediated steroidogenesis has provided insights into a novel negat

183 tion via perturbations in steroid synthesis (steroidogenesis) has become increasingly clear.

184 iduals with an ABS-like phenotype and normal steroidogenesis have FGFR mutations, whereas those with

185 al processes ranging from drug metabolism to steroidogenesis, human microsomal cytochrome P450 enzyme

186 tent with these in vivo data, Wnt4 repressed steroidogenesis in adrenocortical and Leydig cell lines,

187 ovel pathway controlling StAR expression and steroidogenesis in adrenocortical cells.

188 is critical for normal gonadotropin-induced steroidogenesis in both male and female gonads.

189 from IFN-gamma to IL-13 production, linking steroidogenesis in CD8(+) T cells, a nonclassical steroi

190 This dominant negative mutant suppressed steroidogenesis in COS cells expressing the mitochondria

191 estrol (DES) results in major suppression of steroidogenesis in fetal testes.

192 hese in vitro systems and blocked LH-induced steroidogenesis in intact follicles primed with pregnant

193 Steroidogenesis in Leydig cells was unaffected by MMP in

194 ion of the EGFR kinase attenuated LH-induced steroidogenesis in MA-10 Leydig cells.

195 ation of steroidogenesis by delaying maximal steroidogenesis in MA-10 mouse tumor Leydig cells.

196 ds significantly impaired adrenal growth and steroidogenesis in mice.

197 the absence of evidence for de novo androgen steroidogenesis in molluscs, these findings suggest that

198 A-mediated regulation of StAR expression and steroidogenesis in mouse Leydig cells.

199 transition in several animal species, alter steroidogenesis in multiple animal models and women, and

200 rane-bound EGF moieties abrogated LH-induced steroidogenesis in ovarian follicles but not MA-10 cells

201 d our model to predict the time evolution of steroidogenesis in response to physiological adrenocorti

202 new approach for the maintenance of adrenal steroidogenesis in sepsis.

203 investigate the interaction between FAs and steroidogenesis in steroidogenic cells.

204 Here we show that tumors induce de novo steroidogenesis in T lymphocytes to evade anti-tumor imm

205 reconstitution assay, adrenal PMs supported steroidogenesis in the absence of additional transport p

206 evelopment and regulates adrenal and gonadal steroidogenesis in the adult, whereas LRH-1 is a critica

207 ranscripts by an shRNA construct potentiates steroidogenesis in the commonly used Y-1 adrenal cell li

208 conserved regulator of gonadotropin-induced steroidogenesis in the gonads, although the mechanisms o

209 und 8, we investigated the role of CaV1.3 on steroidogenesis in the human adrenocortical cell line, H

210 Furthermore, the retained capacity for steroidogenesis in the mature thalamus raises the prospe

211 uced glucocorticoids and genetic ablation of steroidogenesis in these cells as well as localized phar

212 ion of the EGFR kinase prevented EGF-induced steroidogenesis in these in vitro systems and blocked LH

213 Our results showed that EGF promoted steroidogenesis in two different in vitro models of oocy

214 y, the PDE8 family has been shown to control steroidogenesis in two tissues.

215 eliminated the membranes' ability to support steroidogenesis in vitro and reduced steroid production

216 ARMC5 inactivation decreased steroidogenesis in vitro, and its overexpression altered

217 AP), a polypeptide that regulates testicular steroidogenesis in vitro, we compared the testicular str

218 , but not late (120 min or more), LH-induced steroidogenesis in vitro.

219 rols may play an important role in enhancing steroidogenesis in vivo.

220 induced angiogenesis, cell proliferation and steroidogenesis in wild type luteal cells, whereas the r

221 cal bile acid levels were found to stimulate steroidogenesis independent of FXR and TGR5.

222 ated (i) whether hypoxia can directly affect steroidogenesis independent of pituitary regulation via

223 h exogenous gonadotropins stimulated gonadal steroidogenesis, inducing germ cell maturation in males

224 enefits only a small percentage of patients, steroidogenesis inhibitors, including mitotane, ketocona

225 courtship leks, treated with drugs to block steroidogenesis, injected with (3)H-labeled testosterone

226 Adrenal and gonadal steroidogenesis is controlled by changes in the steroido

227 ng that the cholesterol substrate needed for steroidogenesis is provided by both de novo synthesis an

228 An essential component of regulated steroidogenesis is the translocation of cholesterol from

229 ilization (hpf), a developmental window when steroidogenesis is unregulated by pituitary influence, r

230 and that reactive oxygen is produced during steroidogenesis itself, we hypothesized that long-term s

231 Luteinizing hormone (LH) stimulates steroidogenesis largely through a surge in cyclic AMP (c

232 This disruption in steroidogenesis likely explains the demasculinization of

233 ocortin peptides mediate functions including steroidogenesis, lipolysis, and thermoregulation.

234 n the lung and indicate that defective local steroidogenesis may contribute to the pathogenesis of al

235 We conclude that intracrine steroidogenesis may permit tumors to circumvent low leve

236 Important for ACTH-dependent steroidogenesis, Mc2r, Stard1, and Cypa11a1 levels were

237 e hypothesized that long-term suppression of steroidogenesis might inhibit or prevent age-related def

238 s, whereas other higher K(m) PDE(s) modulate steroidogenesis more effectively when cells are fully st

239 important participant in skin pigmentation, steroidogenesis, obesity, energy homeostasis and exocrin

240 gical functions including skin pigmentation, steroidogenesis, obesity, energy homeostasis, and exocri

241 noviral mutants altered basal and stimulated steroidogenesis of adrenocortical cells.

242 he components of the Hh signaling pathway in steroidogenesis of endocrine tissues.

243 and proteins of steroidogenic machinery and steroidogenesis of gonadotropin-treated hGLC.

244 y obesity have been reported to suppress the steroidogenesis of Leydig cells.

245 tightly linked ovarian processes, including steroidogenesis, oocyte maturation, and ovulation.

246 ved from cholesterol through the traditional steroidogenesis pathway initiated by enzyme CYP11A1, and

247 e anti-tumor immunity, and inhibition of the steroidogenesis pathway is sufficient to restore anti-tu

248 ompassing enzyme deficiencies in the adrenal steroidogenesis pathway that lead to impaired cortisol b

249 e GGM reflects metabolite relations from the steroidogenesis pathway.

250 13-secreting phenotype through regulation of steroidogenesis, potentially governing asthma susceptibi

251 1, demonstrating HSL-dependent regulation of steroidogenesis predominantly involves LXR signaling.

252 take from HDL as a source of cholesterol for steroidogenesis raised the possibility that SR-BI may pa

253 ) treatment of HPX rats maximally stimulated steroidogenesis rates within 5 min with over 10-fold ele

254 At 360 min, steroidogenesis remained elevated, but mRNA, nascent RNA

255 Using a transgenic steroidogenesis-reporter mouse line we identify and char

256 Steroidogenesis requires that 3betaHSD2 acts as both a d

257 Genetic ablation of T cell steroidogenesis restricts primary tumor growth and metas

258 n to lead to defects in bone development and steroidogenesis, resulting in sexual dimorphisms, the se

259 However, whether reduced LC steroidogenesis results from specific effects of aging w

260 hose with ambiguous genitalia and disordered steroidogenesis should be recognized as having a distinc

261 Examination of adrenal and gonadal steroidogenesis showed no defects in Tspo(-/-) mice.

262 ggesting CYP17A1 has a key role in prostatic steroidogenesis similar to testis and adrenal roles.

263 interaction, olfactory transduction, ovarian steroidogenesis, steroid biosynthesis and CAMs signaling

264 s involved in initial steps of mitochondrial steroidogenesis, suggesting conversion of lysosome-deriv

265 ture, a morphological change associated with steroidogenesis, suggesting possible involvements of LD

266 cholesterol augmented, PDE inhibitor-induced steroidogenesis, suggesting that the cholesterol substra

267 on of STX5 and alpha-SNAP from PMs decreased steroidogenesis supported by PMs in vitro.

268 ble system for assessing chemical impacts on steroidogenesis, supporting chemical risk assessment, pr

269 n of reactive oxygen species, a byproduct of steroidogenesis that induces apoptosis, is down-regulate

270 separate events, an initial genetic loss of steroidogenesis that is dependent on steroidogenic acute

271 -3-3gamma isoform is a negative regulator of steroidogenesis that is hormonally induced and transient

272 regulatory protein and a subsequent loss of steroidogenesis that is independent of the protein due t

273 on Factor II (COUP-TFII) in Leydig cell (LC) steroidogenesis that may partly explain this.

274 stingly, although cAMP was always needed for steroidogenesis, the EGFR/MAPK pathway was activated and

275 n intracellular cAMP are known regulators of steroidogenesis, the roles of other signaling pathways i

276 te regulatory protein (STAR) participates in steroidogenesis through the mitochondrial transfer of ch

277 n, suggesting that the PDGF pathway controls steroidogenesis through these genes in both sexes.

278 g 8-bromo-cAMP (8-Br-cAMP), which stimulates steroidogenesis, triggers the interaction of 14-3-3gamma

279 ion of PDE8B as a major regulator of adrenal steroidogenesis using a genetically ablated PDE8B mouse

280 LH and EGF receptor cross-talk in testicular steroidogenesis using mouse MLTC-1 Leydig cells.

281 or of one or more pools of cAMP that promote steroidogenesis via both short- and long-term mechanisms

282 LPV/r in vitro effect on steroidogenesis was assessed in H295R cells.

283 this paper a stoichiometric model of piscine steroidogenesis was constructed and constrained with pro

284 uring human sex-differentiation and onset of steroidogenesis was evaluated by whole-genome expression

285 with MAM-associated proteins, and therefore steroidogenesis was inhibited.

286 The first PDE known to directly regulate steroidogenesis was PDE2, the cGMP-stimulated PDE.

287 a1 mRNA - a key mitochondrial P450 enzyme in steroidogenesis, was stimulated at all doses of UVB irra

288 pheral-type benzodiazepine receptor (PBR) in steroidogenesis, we developed a molecular approach based

289 ic androgen-dependent organs and Leydig cell steroidogenesis were fully restored by administration of

290 receptors and several enzymes of sex hormone steroidogenesis were greater than in control fish.

291 hrome P450 17A1, 19A1, and 21A2, critical in steroidogenesis, were similar using our purified, full-l

292 ed SR-BI-mediated selective CE transport and steroidogenesis, which were markedly attenuated by parti

293 ifications further induced 8-Br-cAMP-induced steroidogenesis while reducing lipid storage, suggesting

294 el, this study advances our understanding of steroidogenesis with broad implications in biology and m

295 d by TOR and feedback signaling that couples steroidogenesis with growth and ensures proper maturatio

296 ism that adjusts cholesterol trafficking and steroidogenesis with nutrition and developmental program

297 to initiate and terminate massive levels of steroidogenesis within a few minutes, permitting the rap

298 We hypothesized that ongoing steroidogenesis within prostate tumors and the maintenan

299 n the MA-10 mouse tumor Leydig cell model of steroidogenesis without any significant toxicity.

300 of TLX1 and that mutations that only impair steroidogenesis, without altering the SF1/SRY transactiv