ライフサイエンスコーパス: Leydig cell

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

2 1A1 and StAR in both H295R adrenal and MA-10 Leydig cells.

3 somatic ovarian cells into functional fetal Leydig cells.

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

5 r gonadotropin-induced steroid production in Leydig cells.

6 esticular steroidogenesis using mouse MLTC-1 Leydig cells.

7 pressed in postmeiotic germ and interstitial Leydig cells.

8 ulation of steroidogenic cells distinct from Leydig cells.

9 n superfamily and is expressed in testicular Leydig cells.

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

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

12 were not induced by steroidogenic stimuli in Leydig cells.

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

14 transcripts in ovarian theca and testicular Leydig cells.

15 AMP-induced androgen formation in testicular Leydig cells.

16 e-induced steroid biosynthesis in testicular Leydig cells.

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

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

19 hat MIS can lower testosterone production by Leydig cells.

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

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

22 tochondrial localization seen in mouse tumor Leydig cells.

23 tosterone and additional factors produced by Leydig cells.

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

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

26 restricted to a second somatic lineage, the Leydig cells.

27 reported to suppress the steroidogenesis of Leydig cells.

28 through the regulation of steroidogenesis by Leydig cells.

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

30 ulate androgen secretion in the interstitial Leydig cells.

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

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

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

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

35 StAR expression and steroidogenesis in mouse Leydig cells.

36 sphodiesterases that are highly expressed in Leydig cells.

37 precursors that can differentiate into fetal Leydig cells.

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

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

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

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

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

43 en identified in kidney, thyroid, pituitary, leydig cell, adrenocortical and, more recently, in color

44 Despite a conserved density of Leydig cells after 30 days of culture (D30), transcript

45 and Fads were also downregulated in cultured Leydig cells after iDKO.

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

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

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

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

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

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

52 The Leydig cells also exhibited a distribution analogous to

53 13 is expressed as a predominant form in the Leydig cell and as a minor form in the ovary and liver.

54 5-e21.5, manifesting as focal aggregation of Leydig cells and ectopic Sertoli cells (SC).

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

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

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

58 there is a lack of spermatogenesis, lack of leydig cells and lack of mature sperm.

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

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

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

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

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

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

65 of culture (D30), transcript levels of adult Leydig cells and steroidogenic markers were decreased.

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

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

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

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

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

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

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

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

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

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

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

77 thway genes are not synchronized among fetal Leydig cells; and some fetal Leydig cells express incomp

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

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

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

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

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

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

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

85 Despite fetal Leydig cells are thought to originate from proliferating

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

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

88 (Sertoli cells, interstitial cells and fetal Leydig cells) between W8 and W15, and this is associated

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

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

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

92 hog signaling and testosterone production in Leydig cells, cell death and growth in testicular peritu

93 c genes (such as Cyp17a1, Star, and Fads) in Leydig cells concomitant with alterations in Sertoli cel

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

95 es in final body weight, reduced Sertoli and Leydig cell counts, and lowered testosterone levels comp

96 The treatment of primary Leydig cell culture with a CDK8/19 inhibitor did not ind

97 ion, this study reports the failure of adult Leydig cell development and altered steroid production a

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

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

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

101 Leydig cells differentiate and produce steroid hormones

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

103 to study the molecular mechanisms underlying Leydig cell differentiation and could be used to treat m

104 ablish Nr2f2 as a crucial regulator of fetal Leydig cell differentiation and provide molecular insigh

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

106 romotes the progenitor fate while suppresses Leydig cell differentiation by modulating key transcript

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

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

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

110 Impaired fetal Leydig cell differentiation leads to differences of sex

111 Leydig cell differentiation was not affected in these tr

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

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

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

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

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

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

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

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

120 In Leydig cell dysfunction, cells respond weakly to stimula

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

122 myoid cells proliferated over time, and that Leydig cell estimates remained stable with physiological

123 zed among fetal Leydig cells; and some fetal Leydig cells express incomplete sets of genes.

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

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

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

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

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

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

130 Fetal Leydig cells (FLCs) play a central role in the synthesis

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

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

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

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

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

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

137 t the peak of the disease, implying that the Leydig cell functional capacity was affected.

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

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

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

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

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

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

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

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

146 l seminiferous tubule atrophy accompanied by Leydig cell hyperplasia was observed and began as early

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

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

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

150 Furthermore, adult males develop Leydig cell hyperplasia.

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

152 Leydig cell hyperproliferation and increased intra-testi

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

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

155 sex development, including dysgenic testes, Leydig cell hypoplasia, cryptorchidism, and hypospadias.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 udies have shown that TSPO declines in aging Leydig cells (LCs) and that its decline is associated wi

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

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

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

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

190 roidogenic cell models, i.e. the mouse tumor Leydig cell line mLTC1, and the human primary granulosa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 erent types of stem cells, for example, stem Leydig cells, mesenchymal stem cells, and pluripotent st

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

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

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

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

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

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

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

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

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

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

216 6 immunoreactivity (irINSL6) was detected in Leydig cells of the mouse testis.

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

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

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

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

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

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

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

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

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

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

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

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

229 The fetal Leydig cell population is restricted by Notch2 signaling

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

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

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

233 Testicular fetal Leydig cells produce androgens essential for male reprod

234 Leydig cells produce testosterone in the testes under th

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

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

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

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

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

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

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

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

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

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

245 nces have been made in the identification of Leydig cell sources for use in transplantation surgery,

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

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

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

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

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

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

252 itial macrophages specifically promote adult Leydig cell steroidogenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 ms governing the interstitial cells to fetal Leydig cell transition remain elusive.

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

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

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

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

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

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

275 Leydig cell tumors are the most frequent interstitial ne

276 Rat Leydig cell tumors grew rapidly in severe combined immun

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

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

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

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

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

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

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

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

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

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

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

288 ement of autophagy in the steroidogenesis of Leydig cells, we treated MA-10 cells with autophagy regu

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

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

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

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

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

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

295 Leydig cells, which normally reside in the peritubular s

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

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

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

299 Treatment of Leydig cells with human chorionic gonadotropin rapidly i

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