ライフサイエンスコーパス: Leydig

1 Leydig cell differentiation was not affected in these tr

2 Leydig cell hyperproliferation and increased intra-testi

3 Leydig cell number and function decline as men age, and

4 Leydig cell numbers were normal on day 1 and day 5 in al

5 Leydig cell tumors are the most frequent interstitial ne

6 Leydig cells (LCs) are thought to differentiate from spi

7 Leydig cells differentiate and produce steroid hormones

8 Leydig cells produce testosterone in the testes under th

9 Leydig cells, which normally reside in the peritubular s

10 Leydig insulin-like hormone (Insl3) is a member of the i

11 esticular steroidogenesis using mouse MLTC-1 Leydig cells.

12 TAT-CRAC efficiently transduced into MA-10 Leydig cells and inhibited the hCG- and cAMP-stimulated

13 Hormone treatment of MA-10 Leydig cells induced the co-localization of TSPO, PAP7,

14 yryl cyclic AMP (Bt(2)cAMP)-stimulated MA-10 Leydig cells were treated with AA and/or the phospholipa

15 Steroidogenic stimulation of mouse MA-10 Leydig cells with dibutyryl-cAMP (Bt2cAMP) resulted in s

16 1A1 and StAR in both H295R adrenal and MA-10 Leydig cells.

17 tenuated LH-induced steroidogenesis in MA-10 Leydig cells.

18 MA-10 Leydig tumor cells stably transfected with either a wild

19 not in TSPO-rich steroidogenic cells (MA-10 Leydig) with high basal Tspo transcriptional activity.

20 vity in TSPO-rich steroidogenic cells (MA-10 Leydig), as well as basal and PMA-induced Tspo promoter

21 ulations during development: fetal and adult Leydig cells (FLCs and ALCs, respectively).

22 ed state during fetal stage and become adult Leydig cells in post-pubertal testis.

23 Leydig cells (FLC) are substituted by adult Leydig cells (ALC) during perinatal testis development.

24 stis development, in particular during adult Leydig cell (ALC) differentiation and function, remains

25 will be a useful marker in studies of adult Leydig cell development.

26 ) is ablated from approximately 75% of adult Leydig stem cell/cell progenitors, from fetal life onwar

27 r perturbed androgen action within the adult Leydig cell lineage predisposes individuals to this late

28 , although how is unknown, because the adult Leydig cells (ALCs) that produce testosterone do not dif

29 n, DINCH exposure appears to directly affect Leydig cell function, likely causing premature aging of

30 is becoming clearer that varicocele affects Leydig cell function as well as seminiferous tubular fun

31 r, we show that cells with mixed adrenal and Leydig cell properties are found dispersed in the inster

32 ressed steroidogenesis in adrenocortical and Leydig cell lines, as evidenced by reduced progesterone

33 he elevated spermatogenic cell apoptosis and Leydig cell hyperproliferation in the Six5-/- mice.

34 of somatic origin, such as Sertoli cell and Leydig cell tumors.

35 Sertoli cells and Leydig cells appear relatively unaffected in mutants.

36 atogonia as well as in pre-Sertoli cells and Leydig cells but was undetectable in spermatocytes and s

37 s of germ cells but spared Sertoli cells and Leydig cells.

38 lium, increased apoptosis of germ cells, and Leydig cell hyperplasia.

39 ownstream of Sry in testis organogenesis and Leydig cell differentiation.

40 mice, atrophic androgen-dependent organs and Leydig cell steroidogenesis were fully restored by admin

41 estosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.

42 gonadal development, and because Sertoli and Leydig cells are located ectopically in the adult, we hy

43 cle, we show that, in testicular Sertoli and Leydig cells, Wnt-4 up-regulates Dax1, a gene known to a

44 Ibuprofen suppressed testosterone and Leydig cell hormone INSL3 during culture of 8-9 GW fetal

45 INSL3, also known as Leydig insulin-like peptide or relaxin-like factor, is a

46 rrogation of the specific roles of autocrine Leydig cell AR signaling through comparison to adjacent

47 ig cells before sexual maturity, and by both Leydig and Sertoli cells thereafter.

48 ligands, Gas6 and protein S, are produced by Leydig cells before sexual maturity, and by both Leydig

49 Recent studies show that INSL3, produced by Leydig cells, and its receptor LGR8 (RXFP2) are essentia

50 tosterone and additional factors produced by Leydig cells.

51 hat MIS can lower testosterone production by Leydig cells.

52 T is synthesized by Leydig cells (LCs), proposed to derive from mesenchymal

53 ading to the induction of testicular cancer (Leydig cell tumors).

54 al tumours (such as juvenile granulosa-cell, Leydig-cell, and Sertoli-cell tumours).

55 toli and granulosa) and steroidogenic cells (Leydig and theca-interstitium) are two major somatic cel

56 through receptors (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.

57 gion of mouse spermatozoa, in Sertoli cells, Leydig cells, and round spermatids in the testis, and in

58 Furthermore, adult males develop Leydig cell hyperplasia.

59 Testes contain two distinct Leydig cell populations during development: fetal and ad

60 l somatic progenitor cells causes a dramatic Leydig cell loss, associated with an increase in undiffe

61 elated to objectively quantified dysgenesis (Leydig cell aggregation) at e21.5 in male fetuses expose

62 er, DBP-induced focal testicular dysgenesis (Leydig cell aggregation, ectopic Sertoli cells, malforme

63 down regulates Insl3 expression in embryonic Leydig cells, thereby providing a mechanism for cryptorc

64 via Silastic implants to suppress endogenous Leydig cell testosterone production.

65 In a previous publication, we examined Leydig cell-specific TSPO conditional knock-out mice tha

66 Also, mice overexpressing MIS exhibited Leydig cell hypoplasia and lower levels of serum testost

67 ome acellular, empty spaces among the extant Leydig cells.

68 ation, mesonephric cell migration, and fetal Leydig cell differentiation.

69 During testis development, fetal Leydig cells increase their population from a pool of pr

70 These ectopic fetal Leydig cells produced androgens and insulin-like growth

71 somatic ovarian cells into functional fetal Leydig cells.

72 because ESR1 is not expressed in human fetal Leydig cells.

73 as expressed in rat, but not in human, fetal Leydig cells.

74 ne encoding activin A, specifically in fetal Leydig cells resulted in a failure of fetal testis cord

75 ether Hh alone is sufficient to induce fetal Leydig cell differentiation, we ectopically activated th

76 The interstitial fetal Leydig cells, however, are thought only to masculinize t

77 precursors that can differentiate into fetal Leydig cells.

78 er genes in the establishment of mouse fetal Leydig cells.

79 dysgenesis and early (during the MPW) fetal Leydig cell dysfunction.

80 uperfamily, as a product of the murine fetal Leydig cells that acts directly upon Sertoli cells to pr

81 Similarly, there was recovery of fetal Leydig cell markers by E14.5, indicating that loss of Sf

82 Neither the origin of fetal Leydig cell precursors nor the signaling pathway that sp

83 ty to phthalate-induced suppression of fetal Leydig cell steroidogenesis.

84 vering an active and essential role of fetal Leydig cells during testis cord morphogenesis.

85 The appearance of fetal Leydig cells was a direct consequence of Hh activation a

86 onads revealed that differentiation of fetal Leydig cells was severely defective.

87 in utero timing for the development of fetal Leydig cells, and hence testosterone production for hypo

88 ing in the origin and specification of fetal Leydig cells.

89 ed in the proliferation or survival of fetal Leydig precursors in the interstitium of the XY gonad.

90 s known about DEHP effects in utero on fetal Leydig cells (FLC).

91 Sf1/Dax1 delays but does not preclude fetal Leydig cell development.

92 monly accepted that androgen-producing fetal Leydig cells (FLC) are substituted by adult Leydig cells

93 o two cell lineages: steroid-producing fetal Leydig cells and non-steroidogenic cells.

94 that active Notch signaling restricts fetal Leydig cell differentiation by promoting a progenitor ce

95 e developing testis, expression of the fetal Leydig cell markers Cyp17 and Cyp11a1 was reduced in het

96 The fetal Leydig cell population is restricted by Notch2 signaling

97 g is dispensable for the attainment of final Leydig cell number but is essential for Leydig cell matu

98 ian failure, 31.1% (95% CI, 27.3%-34.9%) for Leydig cell failure, and 40.9% (95% CI, 32.0%-49.8%) for

99 inal Leydig cell number but is essential for Leydig cell maturation and regulation of steroidogenic e

100 cribe the prevalence of and risk factors for Leydig cell failure (LCF), Leydig cell dysfunction (LCD)

101 dentify a common pre-pubertal progenitor for Leydig and myoid cells and delineate candidate factors c

102 ulation of steroidogenic cells distinct from Leydig cells.

103 actor bombyxin, the relaxin-like factor from Leydig cells, and the insulin-like factor 4 (INSL4) all

104 istological analysis showed the mice to have Leydig cell tumors, unilaterally or bilaterally.

105 p4 is expressed primarily in mouse and human Leydig cells; however, there is no current evidence that

106 differentiation of hiPSCs into either human Leydig-like (hLLCs) or adrenal-like cells (hALCs) using

107 to human relaxin, and 34% identity to human Leydig insulin-like factor.

108 ete testis by Sertoli cells and hyperplastic Leydig cells, leading to seminiferous tubule dilation an

109 stimulator of SSC self-renewal and implicate Leydig and myoid cells as contributors of the testicular

110 In Leydig cells from wild-type mice, 3-isobutyl-1-methylxan

111 seems to be a physiologic target of Dax-1 in Leydig cells, and increased Cyp19 expression may account

112 GR-LACS mRNA is expressed abundantly in Leydig cells of the adult testis and to a lesser degree

113 Increased proliferative activity in Leydig cells was evidenced by enhanced expression of cel

114 pes and gonadotropes of the pituitary and in Leydig and germ cells in the testes, but at very low lev

115 of hypothalamic and brainstem neurons and in Leydig cells of the testis suggests a diverse biological

116 ect important role in spermatogenesis and in Leydig cells plays an autocrine regulatory role to modul

117 Defects in Leydig cell differentiation in Dhh(-/-) XY gonads did no

118 nephric cell migration but caused defects in Leydig cell differentiation.

119 t inhibit or prevent age-related deficits in Leydig cell testosterone production.

120 for testosterone production was detected in Leydig cells isolated from PDE8A knockout mice.

121 6 immunoreactivity (irINSL6) was detected in Leydig cells of the mouse testis.

122 ectomy to prevent or reduce deterioration in Leydig cell function remains unproven, recent data sugge

123 as a 79-kDa cytoplasmic protein expressed in Leydig cells of the rat testis.

124 We report here that PDE8A is expressed in Leydig cells, and using PDE8A knockout mice we provide e

125 sphodiesterases that are highly expressed in Leydig cells.

126 ependent transcription of GRTH expression in Leydig cells is accompanied by a marked increase of 43-k

127 nal down-regulation of GR-LACS expression in Leydig cells.

128 d specific expression of Pkd1l1 was found in Leydig cells, a known source of testosterone production,

129 est whether these elements are functional in Leydig cells, a battery of Plp1-lacZ fusion genes with p

130 ile of various steroidogenic enzyme genes in Leydig cells isolated from Dax1-deficient male mice.

131 in the mouse testis by binding to GPRC6A in Leydig cells.

132 iated mechanism that controls cell growth in Leydig cell tumors.

133 hancer-of-split 1, results in an increase in Leydig cells in the testis.

134 g cell hyperplasia implies a role for Kit in Leydig cell differentiation and/or steroidogenesis.

135 down reduced Tspo mRNA and protein levels in Leydig cells.

136 ve protein expression was observed mainly in Leydig cells and minimally in the tubules but was not de

137 with a typical prolonged washout observed in Leydig cell tumors (12 of 21 patients, P < .001 when com

138 d (ii) the role of the CRAC domain of PBR in Leydig cell steroidogenesis by using a transducible pept

139 n reduced STAT3 and c-Jun phosphorylation in Leydig cells.

140 testis, p130 mRNA is found predominantly in Leydig cells.

141 essential for spermatogenesis, is present in Leydig cells (LC) and germ cells.

142 in-regulated RNA helicase that is present in Leydig cells (LCs) and germ cells and is essential for s

143 in-regulated RNA helicase that is present in Leydig cells and germ cells (meiotic spermatocytes and s

144 r the types and roles of the PDEs present in Leydig cells have not been fully defined.

145 or in combination with other PDEs present in Leydig cells, may be exploited to modulate testosterone

146 r gonadotropin-induced steroid production in Leydig cells.

147 TH as a developmentally regulated protein in Leydig cells and in germ cells (pachytene spermatocytes

148 The increase in GRTH 43-kDa protein in Leydig cells caused by hCG treatment was prevented by th

149 l surface divalent cation (Ca2+) receptor in Leydig cells, the activation of which triggers Ca2+ flux

150 eroidogenic "hibernation," the reductions in Leydig cell testosterone production that invariably acco

151 thing is known about Plp1 gene regulation in Leydig cells, which is the focus of this study.

152 We investigated its role in Leydig cells, where testosterone production is regulated

153 rtance of properly regulated Hh signaling in Leydig cell development and testicular functions.

154 tudies reveal that autocrine AR signaling in Leydig cells protects against late-onset degeneration of

155 Steroidogenesis in Leydig cells was unaffected by MMP inhibitors, suggestin

156 were not induced by steroidogenic stimuli in Leydig cells.

157 moter-Transcription Factor II (COUP-TFII) in Leydig cell (LC) steroidogenesis that may partly explain

158 vision I) and round spermatids and weakly in Leydig cells (somatic cells outside of the seminiferous

159 led primary testicular defects that included Leydig cell hyperplasia (LCH) and progressive degenerati

160 ic cells of the developing gonads, including Leydig cells in the testes and granulosa cells in the ov

161 adult testosterone (T) levels and increased Leydig cell numbers.

162 or, decreasing aromatase expression, induces Leydig tumor regression both in vitro and in vivo, sugge

163 seminiferous epithelium in mice and inhibits Leydig cell apoptosis in both adult mice and patients wi

164 wo orphan LGRs, LGR7 and LGR8, whereas INSL3/Leydig insulin-like peptide specifically activates LGR8.

165 es weights were comparable suggesting intact Leydig cell androgen production.

166 pressed in postmeiotic germ and interstitial Leydig cells.

167 ent in peritubular myoid cells, interstitial Leydig cells, vascular endothelial cells and germ cells,

168 ulate androgen secretion in the interstitial Leydig cells.

169 ked whether hAd-PSCs could be converted into Leydig-like cells and determined their capacity to promo

170 uding ectopic Sertoli cells and intratubular Leydig cells (ITLCs).

171 risk factors for Leydig cell failure (LCF), Leydig cell dysfunction (LCD), and associated adverse he

172 karos in skate also is found in the lymphoid Leydig organ and epigonal tissues, which are unique to c

173 When HeLa and MA10 Leydig cells were lipid-loaded, significant levels of AD

174 cAMP-dependent phosphorylation sites in MA10 Leydig cells suggested that cAMP regulates multiple step

175 olic fractions of HeLa cells and murine MA10 Leydig cells grown in low lipid-containing culture mediu

176 f alternative approaches to restore/maintain Leydig cell (LC) androgen production.

177 decreased testosterone production by mature Leydig cells in vivo, we treated luteinizing hormone (LH

178 ays an autocrine regulatory role to modulate Leydig cell steroidogenic function.

179 the hCG-dependent steroidogenic MA-10 mouse Leydig cell line, the 14-3-3gamma protein was identified

180 We demonstrate in MA-10 mouse Leydig cells that activation of the protein kinase A (PK

181 transcriptional activity in both MA-10 mouse Leydig tumor cells and NIH/3T3 whole mouse embryo fibrob

182 uman embryonic kidney cells (EBNA) and mouse Leydig- (TM3) and Sertoli-derived (TM4) cell lines, but

183 StAR expression and steroidogenesis in mouse Leydig cells.

184 zed by expressing the mutant enzyme in mouse Leydig MA-10 cells and assaying 1alpha-hydroxylase activ

185 2+]) was investigated in fura-2-loaded mouse Leydig (TM3) cells.

186 erone conversion in both steroidogenic mouse Leydig MA-10 and human adrenal NCI cells.

187 on 1 sequence was transfected into the mouse Leydig cell line, TM3.

188 distinct from the binding pattern with mouse Leydig cell nuclear proteins.

189 terone biosynthesis was reduced in Mrp4(-/-) Leydig cells in vivo.

190 ions, such as cardiac and skeletal myocytes, Leydig cells, prostatic epithelium, and salivary serous

191 Therefore, Mrp4 is required for normal Leydig cell testosterone production.

192 5-e21.5, manifesting as focal aggregation of Leydig cells and ectopic Sertoli cells (SC).

193 Direct assessment of Leydig cell function in childhood cancer survivors has b

194 nd adult testes was localized to clusters of Leydig cells and select peritubular myoid cells.

195 e infertile group showed variable degrees of Leydig cell hyperplasia, apoptosis of germ cells, sperma

196 a result of MIS affecting the development of Leydig cells or their capacity to produce testosterone.

197 ovary appears to suppress the development of Leydig cells; consequently, Wnt-4-mutant females ectopic

198 d testicular testosterone, and disruption of Leydig cell cAMP homeostasis.

199 Therefore, the failure of Leydig cells to produce testosterone is not secondary to

200 s and the development and lifelong health of Leydig cells.

201 han in control rats, indicating induction of Leydig cell hyperplasia.

202 ficient mice are adequate for maintenance of Leydig cell steroidogenesis and fertility because of par

203 xcept for a slight increase in the number of Leydig cells.

204 The numbers of Leydig cells in the testis of DEHP-treated rats were 40-

205 tion of germ cell meiosis, and regulation of Leydig cell differentiation.

206 ng hormones, and 8.52-fold increased risk of Leydig cell failure.

207 onephros, thought to be a possible source of Leydig cell precursors.

208 ght be a potential target for the therapy of Leydig cell tumors.

209 nd proliferative defects similar to those of Leydig cell-specific activin betaA knockout testes.

210 Moreover, the transfection of Leydig tumor cells with precursor miRNA 125a (pre-miRNA-

211 Treatment of Leydig cells with human chorionic gonadotropin rapidly i

212 esticular and tubular atrophy, oligospermia, Leydig cell hyperproliferation and increased follicle st

213 nephric cell migration, and had no effect on Leydig cell differentiation.

214 tal day 60, indicating a long-term effect on Leydig cells of the testis.

215 hat varicoceles exert deleterious effects on Leydig cells, Sertoli cells, and germ cells via very dif

216 TM (seminoma in six, mixed germ cell in one, Leydig cell in two), and three (0.3%) of 884 with no TM

217 ll/cell progenitors, from fetal life onward (Leydig cell AR knockout mice), permitting interrogation

218 ound in boys with Leydig cell hyperplasia or Leydig cell adenomas.

219 e to normal testis control, nonseminomas, or Leydig tumor cells.

220 he development of testis and, in particular, Leydig cells.

221 Androgen receptor-positive Leydig, Sertoli, and some peritubular myoepithelial cell

222 In Mrp4(-/-) primary Leydig cells treated with LH, intracellular cAMP product

223 f ARA70 in the testosterone and E2-producing Leydig cells may enhance the overall activity of AR duri

224 Establishment of the steroid-producing Leydig cell lineage is an event downstream of Sry that i

225 males have decreased testes size, prominent Leydig cell hypoplasia, defects in expression of genes e

226 A Young testicular microenvironment protects Leydig cells against age-related dysfunction in a mouse

227 Stable transfection of the PBR-negative R2C Leydig cells with a vector containing the PBR cDNA resul

228 Rat Leydig cell tumors grew rapidly in severe combined immun

229 CRFR cDNAs derived from rat Leydig cell mRNA included the pituitary Form A, which sp

230 GRTH cloned from rat Leydig cell, mouse testis, and human testis cDNA librari

231 methasone, reduces cell proliferation in rat Leydig tumor cells by decreasing the expression and the

232 severe combined immune deficiency mouse/rat Leydig cell tumor model was developed for testing SC-684

233 n the constitutive steroid producing R2C rat Leydig tumor cell line.

234 tracts from R2C cells, an MIS-responsive rat Leydig cell line that expresses endogenous MISRII, with

235 al AR or FSHR ablation significantly reduced Leydig cell numbers but Sertoli cell specific AR ablatio

236 We conclude that AGD, reflecting Leydig cell function solely within the MPW, is strongly

237 However, the mechanism that regulates Leydig stem cell self-renewal and differentiation is unk

238 through comparison to adjacent AR-retaining Leydig cells, testes from littermate controls, and to hu

239 wer testosterone production by mature rodent Leydig cells and suggest that MIS-mediated down-regulati

240 In testis, RA acts directly in Sertoli, Leydig and pre-meiotic germ cells.

241 ecularly defined the development of Sertoli, Leydig and peritubular myoid cells during the perinatal

242 teosarcoma and in one patient with a Sertoli-Leydig cell tumor.

243 s were seen in hemangioendothelioma, Sertoli-Leydig cell tumor, and fibrosarcoma, respectively.

244 arian tumors (29%), predominantly in Sertoli-Leydig cell tumors (26 of 43, or 60%), including 4 tumor

245 GRTH is produced in both somatic (Leydig cells) and germinal (meiotic spermatocytes and ro

246 cause, leads to malfunction of the somatic (Leydig, Sertoli) cells and consequent downstream TDS dis

247 Stem Leydig cell (SLC) transplantation shows promise in this

248 matic increase in SR-BI in the steroidogenic Leydig cells of the testes.

249 seminiferous tubules, whereas steroidogenic Leydig cells and other less well characterized cell type

250 We found that LH stimulates Leydig insulin-like 3 (INSL3) transcripts in ovarian the

251 res the ability of the previously suppressed Leydig cells to produce testosterone.

252 Testicular Leydig cells (LCs) are the primary source of circulating

253 tion in renal proximal tubule and testicular Leydig cells, and apoptosis in the testis and intestine)

254 ells, renal epithelial cells, and testicular Leydig cells, whereas the testicular or germinal angiote

255 transcripts in ovarian theca and testicular Leydig cells.

256 cells, mammary ductal epithelium, testicular Leydig cells, serous acinar cells of salivary gland, Pan

257 casionally 72, 90, and 110 kDa in testicular Leydig and breast cancer cells.

258 n superfamily and is expressed in testicular Leydig cells.

259 AMP-induced androgen formation in testicular Leydig cells.

260 e-induced steroid biosynthesis in testicular Leydig cells.

261 velop hyperplasia of interstitial testicular Leydig cells, which produce reduced levels of testostero

262 a relaxin family member expressed in testis Leydig cells and ovarian theca and luteal cells.

263 y between flies and mice, and indicates that Leydig cells may be the direct target of Dhh signaling.

264 t harbor Plp1-lacZ fusion genes suggest that Leydig cells are the source of Plp1 gene expression in t

265 The Leydig cell hyperplasia implies a role for Kit in Leydig

266 e lost from the seminiferous tubules and the Leydig cell population is reduced.

267 e relaxin-like factor (RLF), produced by the Leydig cells, is an essential link in the chain of event

268 ed by reduced testosterone production by the Leydig cells, the testosterone-producing cells of the te

269 nd to hCG stimulation but do not express the Leydig specific marker Insl3 showing that they are a pop

270 laris of the adrenal cortex, but also in the Leydig cell, kidney and liver, suggest it may have a rol

271 cyclic AMP-induced androgen formation in the Leydig cell.

272 day 0 during estradiol synthesis and in the Leydig cells at postpartum day 49.

273 stradiol, was increased significantly in the Leydig cells isolated from mutant mice, whereas the expr

274 G protein-coupled receptor expressed in the Leydig cells of the testes, osteocalcin regulates in a C

275 In the testis, TIMP-2 was present in the Leydig cells, and in the brain, it was expressed in pia

276 gh expression of EG-VEGF was detected in the Leydig-like hilus cells found in the highly vascularized

277 on gonads, suggesting that regulation of the Leydig/interstitial cell population is important for mal

278 Thus, by placing the Leydig cells in a state of steroidogenic "hibernation,"

279 e 13 and 23 months of age, respectively, the Leydig cells in both cases were found to produce testost

280 nor the signaling pathway that specifies the Leydig cell lineage is known.

281 ation localizes the regulatory events to the Leydig cell plasma membrane.

282 d testosterone associated with damage to the Leydig cells of the testis.

283 cell function (Sox9, Mis and Dhh) and three Leydig cell steroid biosynthetic enzymes (p450scc, 3beta

284 to the acrosome of spermatids, as well as to Leydig cells in the mouse testis.

285 nced green fluorescent protein expression to Leydig cells of the testis, theca cells of the ovary, an

286 ts suggest that DHH/PTCH1 signaling triggers Leydig cell differentiation by up-regulating Steroidogen

287 esterone production in the MA-10 mouse tumor Leydig cell model of steroidogenesis without any signifi

288 gi apparatus and mitochondria in mouse tumor Leydig cells, in agreement with its proposed function in

289 tochondrial localization seen in mouse tumor Leydig cells.

290 maximal steroidogenesis in MA-10 mouse tumor Leydig cells.

291 this isoform is expressed only by adult-type Leydig cells in the mouse testis and that this developme

292 ice), to analyze interactions between viable Leydig cells (LCs) and testicular macrophages that may l

293 testis as it develops and are activated when Leydig cells differentiate.

294 ntained major proteins of 61/56 kDa, whereas Leydig cells utilized preferentially the 2nd ATG codon (

295 ion mutations of the hLHR found in boys with Leydig cell hyperplasia or Leydig cell adenomas.

296 In a patient with Leydig cell hypoplasia, we identified a mutant LH recept

297 nclude that autocrine androgen action within Leydig cells is essential for the lifelong support of sp

298 contrast, cBD-2 was located primarily within Leydig cells.

299 PF-04957325 treatment of WT Leydig cells or MA10 cells increased steroid production

300 uce testosterone at the high levels of young Leydig cells, whereas significantly lower levels were pr