ライフサイエンスコーパス: SF-1

1 SF-1 ChIP-on-chip was performed in NCI-H295R human adren

2 SF-1 immunoreactivity was also detected in the exocrine

3 SF-1 is a key transcription factor for all steroidogenic

4 SF-1 is a transcription factor that controls the develop

5 SF-1 is an essential factor for sex determination during

6 SF-1 is the target of both phosphorylation and SUMOylati

7 SF-1 neurons were visualized by Tau-green fluorescent pr

8 SF-1 phosphorylation at these sites is therefore not ess

9 SF-1 transcriptional activity was also differentially re

10 SF-1 was recently shown to interact with DAX-1, another

11 SF-1, an orphan member of the nuclear hormone receptor g

12 mily, which includes steroidogenic factor 1 (SF-1) and liver receptor homolog 1 (LRH-1), regulate cru

13 Here, we report that steroidogenic factor 1 (SF-1) and liver receptor homolog 1 are repressed via pos

14 6b1 is maintained by Steroidogenic Factor 1 (SF-1) and Sex-Determining Region Y Box-9 (SOX9), which e

15 cipation of multiple steroidogenic factor 1 (SF-1) elements with the downstream cAMP response element

16 we first reveal that steroidogenic factor 1 (SF-1) green fluorescent protein (GFP)-positive neurons i

17 Steroidogenic factor 1 (SF-1) is a transcription factor expressed in the ventral

18 Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor selectively expresse

19 Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor that serves as an es

20 Steroidogenic factor 1 (SF-1) is an orphan nuclear receptor with no known ligand

21 The nuclear receptor steroidogenic factor 1 (SF-1) is essential for adrenal development and steroidog

22 The nuclear receptor steroidogenic factor 1 (SF-1) is essential for steroidogenic gene transcription.

23 transcription factor steroidogenic factor 1 (SF-1) is exclusively expressed in the brain in the ventr

24 tral nervous system, steroidogenic factor 1 (SF-1) is required for terminal differentiation of neuron

25 their expression in steroidogenic factor 1 (SF-1) knock-out mice.

26 ice lacking FOXO1 in steroidogenic factor 1 (SF-1) neurons of the VMH are lean due to increased energ

27 han nuclear receptor steroidogenic factor 1 (SF-1) regulates the differentiation and function of endo

28 criptional regulator Steroidogenic Factor 1 (SF-1), and zG-specific Sf-1 deletion prevents lineage co

29 an nuclear receptor, steroidogenic factor 1 (SF-1), which can be detected in the hypothalamic primord

30 ly related receptor steroidogeneic factor 1 (SF-1).

31 han nuclear receptor steroidogenic factor 1 (SF-1).

32 The steroidogenic factor 1 (SF-1, also known as NR5A1) is a transcription factor bel

33 transcription factor steroidogenic factor 1 (SF-1; also known as NR5A1) is a crucial mediator of both

34 1 (LRH-1; NR5A2) and steroidogenic factor 1 (SF-1; NR5A1) have therapeutic potential for the treatmen

35 vely active receptor steroidogenic factor 1 (SF-1; NR5A1), is proposed to repress their transcription

36 anscription factors, steroidogenic factor-1 (SF-1) and early growth response-1 (Egr-1), play a centra

37 Steroidogenic factor-1 (SF-1) and liver receptor homologue-1 (LRH-1) belong to t

38 han nuclear receptor steroidogenic factor-1 (SF-1) are occupied in vitro by using nuclear extracts fr

39 heterozygous for the steroidogenic factor-1 (SF-1) gene suggested that reduced expression of this nuc

40 The nuclear receptor steroidogenic factor-1 (SF-1) has been implicated as a downstream effector of pe

41 phorylation state of steroidogenic factor-1 (SF-1) in mediating ACTH/cAMP-dependent transcription of

42 Steroidogenic factor-1 (SF-1) is an orphan nuclear receptor that binds DNA as a

43 the orphan receptor steroidogenic factor-1 (SF-1) was found to potently transactivate the SHP promot

44 ses transcription by steroidogenic factor-1 (SF-1), a factor that regulates expression of multiple st

45 through synergy with steroidogenic factor-1 (SF-1), a protein required for gonadotrope function.

46 in-alpha, aromatase, steroidogenic factor-1 (SF-1), cholesterol side chain (SCC), and epiregulin.

47 ft analyses a distal steroidogenic factor-1 (SF-1)-binding site that is essential for full promoter a

48 to LC expression of steroidogenic factor-1 (SF-1)-dependent genes (StAR, Cyp11a1, Cyp17a1) with over

49 7-OHC each increased steroidogenic factor-1 (SF-1)-mediated StAR gene transactivation by approximatel

50 omolog-1 (LRH-1) and steroidogenic factor-1 (SF-1).

51 omolog-1 (LRH-1) and steroidogenic factor-1 (SF-1).

52 The nuclear receptor steroidogenic factor-1 (SF-1, NR5A1) is a key regulator of adrenal and gonadal b

53 ctions, as marked by steroidogenic factor-1 (SF-1; NR5A1).

54 as been grouped into helicase superfamily 1 (SF-1).

55 In many Superfamily-1 (SF-1) DNA helicases, helicase sequence motif III links t

56 ures of human NR5A1 (steroidogenic factor-1, SF-1) ligand binding domain (LBD) bound to PIP2 and PIP3

57 a repressor of SF-1 activity, reduced Egr-1-SF-1 synergy and diminished GnRH stimulation of the LHbe

58 activity studies led to excellent dual-LRH-1/SF-1 agonists (e.g., RJW100) as well as compounds select

59 1 and STAT3) inhibitors, BP-1-107, BP-1-108, SF-1-087, and SF-1-088.

60 The apparent absence of a SF-1 ligand prompted speculation that this receptor is r

61 hydrogen bonds with the phospholipid abolish SF-1/coactivator interactions and significantly reduce S

62 as the presence or absence of serum, affect SF-1 action.

63 very active compounds, particularly against SF-1.

64 tion of cyclin D2, aromatase, inhibin-alpha, SF-1, and epiregulin.

65 Although SF-1 is constitutively active in cell-based assays, it i

66 raised by steroid receptor coactivator 1, an SF-1 coactivator.

67 tivities were similarly lowered by DAX-1, an SF-1 suppressor, and raised by steroid receptor coactiva

68 eir promoter regions, but does not affect an SF-1 dependent LC gene (3beta-HSD) without overlapping s

69 ia, suggesting that Dax-1 may function as an SF-1 coactivator under some circumstances.

70 ain-derived neurotrophic factor (bdnf) as an SF-1 target gene, we assessed the colocalization of SF-1

71 oreover, similar effects were observed in an SF-1/thyroid hormone LBD chimera receptor, illustrating

72 function phenotype exhibited by an analogous SF-1 human mutant.

73 nhibitors, BP-1-107, BP-1-108, SF-1-087, and SF-1-088.

74 DAX-1 and SF-1 are members of the orphan nuclear receptor superfam

75 determine the functional roles of DAX-1 and SF-1 in human skin.

76 a distinctive staining pattern for DAX-1 and SF-1 in skin and its appendages.

77 conclude that the synergy between Egr-1 and SF-1 is essential for GnRH stimulation of the LHbeta gen

78 LRH-1 and SF-1 modulators are highly sought as treatments for meta

79 sis demonstrated the expression of DAX-1 and SF-1 mRNA in whole human skin and Western analysis also

80 Co-localization of DAX-1 and SF-1 was demonstrated by immunocytochemistry in the HaCa

81 ith functional selectivity between LRH-1 and SF-1.

82 fied as a high-affinity ligand for LRH-1 and SF-1.

83 us to investigate the presence of DAX-1 and SF-1.

84 various SF-1 target genes and that ASAH1 and SF-1 colocalize on the same promoter region of the CYP17

85 markers of the ventral thyrotrope cells and SF-1-expressing cells of gonadotrope lineage.

86 The NHR-25 homologs Ftz-F1 in Drosophila and SF-1 in mammals are involved in various biological proce

87 activity with JNK/c-Jun phosphorylation and SF-1-dependent Cyp11a1 transcription for steroid synthes

88 promoter in a highly repetitive region, and SF-1-dependent activation was confirmed in luciferase as

89 s compounds selective for LRH-1 (RJW101) and SF-1 (RJW102 and RJW103).

90 both PIAS-dependent receptor sumoylation and SF-1 relocalization to discrete nuclear bodies.

91 enin of other transcription factors, such as SF-1 and C/EBPalpha.

92 al capacity of transcription factors such as SF-1 and is leveraged during development to achieve cell

93 chanism by which SUMO conjugation attenuates SF-1 activity was found to be largely histone deacetylas

94 members of this superfamily, such as NGFI-B, SF-1, and ROR, could also recognize unique geometric fea

95 genesis, but until now a direct link between SF-1 and vascular remodeling has not been established.

96 t coordinates the functional synergy between SF-1 and Egr-1.

97 sal gene, Dax-1, antagonizes synergy between SF-1 and WT1, most likely through a direct interaction w

98 -1 produced in vitro indicate F2 and F3 bind SF-1; BLAST searches and Southwestern blotting suggest t

99 Both SF-1 and Dax-1 bind to steroid receptor RNA activator (S

100 ta promoter but only in the presence of both SF-1 and Egr-1, and not in the presence of other Egr pro

101 Mutation of both SF-1 sites greatly inhibited luciferase expression, wher

102 d that MIP-2A physically interacts with both SF-1 and Ptx1, thereby inhibiting transactivation of the

103 nce of transcriptional programs regulated by SF-1 in the VMH is not well defined.

104 vation cell-based assay employing a chimeric SF-1 construct.

105 s with Dax-1 and synergistically coactivates SF-1 target gene transcription.

106 primarily in the ventrolateral VMH coexpress SF-1 and BDNF, and in contrast to other brain regions, b

107 These data define two composite SF-1-Egr-1 response-elements in the proximal LHbeta gene

108 The compounds SF-1-066 and BP-1-102 are predicted to bind to the STAT3

109 The R103Q mutation decreased SF-1 transactivation of TLX1, a transcription factor tha

110 hat Dax-1 can function as a dosage-dependent SF-1 coactivator.

111 Moreover, phosphorylation-dependent SF-1 activation is likely mediated by the mitogen-activa

112 Mutational analysis of this new distal SF-1 site and the previously identified proximal SF-1 si

113 ering affinities, indicating that the distal SF-1 site is bound more avidly than is the proximal SF-1

114 Mutation of the binding sites for either SF-1 or Egr-1 completely abolishes the synergy between t

115 Here, we permanently eliminated SF-1/NR5A1 sumoylation in mice (Sf-1(K119R, K194R, or 2K

116 ulted in continuing activation by endogenous SF-1, indicating redundancy.

117 tment, loss of SUMOylation leads to enhanced SF-1 phosphorylation at serine 203.

118 or show elevated levels of well-established SF-1 target genes.

119 We therefore examined SF-1 heterozygous (+/-) mice as a potential model for de

120 Introduction of exogenous SF-1 generated cAMP stimulation of the FUER in 10T1/2 fi

121 bryonic kidney (HEK)293 cells do not express SF-1.

122 Steroidogenic factor-1-expressing (SF-1-expressing) neurons in the ventromedial hypothalamu

123 Steroidogenic factor SF-1, a constitutively active nuclear hormone receptor,

124 ns of the gene-encoding transcription factor SF-1.

125 that the SHP promoter contains at least five SF-1 binding sites, and mutagenesis studies demonstrate

126 For SF-1, we find that this intramolecular association and h

127 Sphingosine (SPH) is a ligand for SF-1.

128 hree strongest binding sites is required for SF-1 transactivation.

129 ike transcription factor, a binding site for SF-1 is present only in the promoter 1b active in the ov

130 Cyp17a1) with overlapping binding sites for SF-1 and COUP-TFII in their promoter regions, but does n

131 Regulatory ligands are unknown for SF-1 and LRH-1.

132 ng in a mechanistically distinct manner from SF-1 helicases.

133 function, the mouse PI lacks the functional SF-1 element and hence is inactive.

134 We propose that this novel GPR30/SF-1 pathway increases local concentrations of estrogen,

135 for three other NR5A members-mouse and human SF-1 and human LRH-1-which reveal that these receptors b

136 the putative ligand-binding domains of human SF-1 at 2.1-A resolution and human LRH-1 at 2.5-A resolu

137 for this poorly understood cluster of human SF-1 mutations and demonstrates how signaling phosphoino

138 These results suggest that human SF-1 and LRH-1 may be ligand-binding receptors, although

139 rvation significantly decreased hypothalamic SF-1 levels by promoting ubiquitin-dependent degradation

140 the transcriptional activity of hypothalamic SF-1 was activated by SUMO, but this was attenuated duri

141 t sumoylation at Lys194 would greatly impact SF-1 function, the conformation and coregulator recruitm

142 In contrast, adrenal deficits in SF-1 heterozygotes are revealed under stressful conditio

143 Surprisingly, Ptpn1 deletion in SF-1 neurons caused an age-dependent increase in adiposi

144 X4 receptor-mediated GABAergic depression in SF-1 GFP-positive neurons.

145 usly defined proximal activation function in SF-1 showed that the activation function mapped fully to

146 finity is compromised either by mutations in SF-1 or by sequence alterations in its binding site.

147 adal agenesis in mice with null mutations in SF-1.

148 Daxx participated in SF-1-dependent Cyp11a1 expression as shown by experiment

149 ng in VMH neurons from mice lacking PTP1B in SF-1 neurons.

150 est that increased insulin responsiveness in SF-1 neurons can overcome leptin hypersensitivity and en

151 GABA from the developing VMH is not seen in SF-1 knockout mice, and cells that are immunoreactive fo

152 everal reported SF-1 target genes, including SF-1 itself, was inhibited by treatment with AC-45594 an

153 and discusses SRY and other genes, including SF-1, WT1, DAX-1, and SOX9, that play key developmental

154 hytoestrogen genistein were able to increase SF-1 transcription, promote Ishikawa cell proliferation,

155 Because 7alpha,27-OHC was unable to increase SF-1-dependent StAR promoter activity, we examined 27-OH

156 ders of adrenal development, while increased SF-1 dosage has been associated with adrenocortical tumo

157 e data suggest that, directly or indirectly, SF-1 plays important roles in determining the distributi

158 ts suggested that MIP-2A expression inhibits SF-1- and Ptx1-mediated transactivation of LHbeta promot

159 The activation requires an intact SF-1 RE and is independent of TCF/Lef.

160 A 1.1-kb SF-1-binding region was identified in the angiopoietin 2

161 , but is also expressed in tissues that lack SF-1, including liver.

162 c functional assay employing the full-length SF-1 protein and its native response element, yielding I

163 a knockin mouse model to show that SUMO-less SF-1 binds and activates inappropriate targets, causing

164 pressors to DNA-bound nuclear receptors like SF-1, thereby extending the range of corepressor action.

165 In males, SF-1 participates in sexual development by regulating ex

166 Here we show that maximal SF-1-mediated transcription and interaction with general

167 ore, we examined whether MIP-2A can modulate SF-1- and Ptx1-mediated transcriptional activation.

168 spholipid is readily exchanged and modulates SF-1 interactions with coactivators.

169 Thus multiple SF-1- and GATA-4-binding sites in the MIS promoter are r

170 quence triplet, eliminated binding by mutant SF-1 to all response elements tested.

171 However, mutant SF-1 bound to a subset of response elements containing a

172 ictate DNA binding specificity by the mutant SF-1.

173 mutant was markedly impaired for most native SF-1 response elements.

174 Strikingly, the VMH is absent in newborn SF-1 knockout mice, suggesting that SF-1 is essential fo

175 elective loss of DNA binding to noncanonical SF-1 targets, such as inhibinalpha; this binding deficit

176 Furthermore, GnRH stimulated Egr-1 but not SF-1 expression in LbetaT2 cells.

177 -1, the modification inhibits the ability of SF-1 to activate target genes.

178 have previously demonstrated the ability of SF-1 to bind to and transactivate the rat LHbeta gene pr

179 Thus, the absence of SF-1 profoundly affects the cellular architecture of the

180 pment as evidenced by both the activation of SF-1-dependent transcription in the adrenal cortex by si

181 es reduced the transcriptional activities of SF-1 and LRH-1 in mammalian cell transfection assays wit

182 t alterations in the levels or activities of SF-1 or FTF could modulate SHP expression in appropriate

183 t HIPK3 action to potentiate the activity of SF-1 for Cyp11a1 transcription in mouse adrenocortical Y

184 -1 represses the transcriptional activity of SF-1, and AHC mutants of DAX-1 lose repression function.

185 r repressing the transcriptional activity of SF-1.

186 the StAR promoter indicates that blockade of SF-1 SUMOylation leads to an increase in overall promote

187 rget gene, we assessed the colocalization of SF-1 and BDNF expressing neurons, as well as expression

188 he functional and structural consequences of SF-1 sumoylation at two conserved lysines (Lys119 and Ly

189 litude of GABAergic postsynaptic currents of SF-1 GFP-positive neurons.

190 erentiates into a neuronal cluster devoid of SF-1.

191 Disruption of SF-1 can lead to disorders of adrenal development, while

192 ns, demonstrating that normal gene dosage of SF-1 is required for mounting an adequate stress respons

193 alamic development and will be downstream of SF-1, a critical factor for normal VMH differentiation.

194 The enhancement of SF-1 activity by Daxx required JNK and c-Jun phosphoryla

195 osis motif enhances neuronal excitability of SF-1 GFP-positive neurons.

196 proximal (P)-box of the first zinc finger of SF-1 (G35E) has been reported to cause complete XY sex r

197 ntially to the SUMOylation-deficient form of SF-1 and that CDK7 inhibition reduces phosphorylation of

198 R) mice failed to phenocopy a simple gain of SF-1 function or show elevated levels of well-establishe

199 hough serine phosphorylation of the hinge of SF-1 (NR5A1), the closest relative of LRH-1, confers a s

200 itions, further supporting the importance of SF-1 in the control of energy homeostasis.

201 ed modification model in which inhibition of SF-1-mediated transcription by SUMOylation in adrenocort

202 es not alter the subcellular localization of SF-1, the modification inhibits the ability of SF-1 to a

203 However, the molecular mechanisms of SF-1 in the control of energy balance are largely unknow

204 We propose that this single modification of SF-1 and the subsequent recruitment of nuclear receptor

205 Thus, pharmacological modulation of SF-1 is critical to its function as an endocrine master

206 he therapeutic potential and pharmacology of SF-1 still remains elusive.

207 nita (AHC), which resembles the phenotype of SF-1-deficient mice.

208 t CDK7 inhibition reduces phosphorylation of SF-1.

209 ough reduced CDK7-induced phosphorylation of SF-1.

210 to investigate the therapeutic potential of SF-1.

211 n of selective inhibitory chemical probes of SF-1 by a rational ultra-high-throughput screening (uHTS

212 tion play crucial roles in the regulation of SF-1 function and that these effects are dependent on nu

213 However, liver expresses a close relative of SF-1, the orphan fetoprotein transcription factor (FTF),

214 derived lipids, is part of the repertoire of SF-1-responsive genes involved in steroidogenesis.

215 t the nuclear receptor DAX-1, a repressor of SF-1 activity, reduced Egr-1-SF-1 synergy and diminished

216 To delineate the functional significance of SF-1 itself in the brain, we generated pre- and postnata

217 We aimed to identify a novel subset of SF-1 target genes in the adrenal by using chromatin immu

218 2 as a potentially important novel target of SF-1 in the adrenal gland, indicating that regulation of

219 r whose tissue distribution overlaps that of SF-1.

220 These data extend our understanding of SF-1 function within steroidogenic tissues and suggest t

221 osphorylation sites (Ser-430 and Ser-203) on SF-1 had no effect on the SF-1-dependent FUER stimulatio

222 ction by directly binding to the receptor on SF-1 target gene promoters and identify a key role for n

223 This surface on SF-1 coincides with the predicted binding site of the co

224 entified regulatory protein-lipid surface on SF-1 with the phosphoinositide head group at its nexus a

225 be mutually exclusive, suggesting that once SF-1 is bound to DNA, sumoylation may be less important

226 Mutation of either Egr-1 or SF-1 elements within the LHbeta promoter attenuated this

227 ted by HIPK3, lost the ability to potentiate SF-1 activity for Cyp11a1 expression.

228 Furthermore, preventing SF-1 SUMOylation increases the mRNA and protein levels o

229 ates, PIASy and PIASxalpha strongly promoted SF-1 sumoylation, and addition of DP103 enhanced both PI

230 site and the previously identified proximal SF-1 site showed that both are necessary for transcripti

231 te is bound more avidly than is the proximal SF-1 site.

232 ork analysis of genes identified as putative SF-1 targets revealed enrichment for angiogenic process

233 osed ligand for the nuclear hormone receptor SF-1 (NR5A1).

234 is regulated by the orphan nuclear receptor SF-1 and homeodomain protein Ptx1.

235 addition, we identified the nuclear receptor SF-1 as a direct FOXO1 transcriptional target in the VMH

236 The orphan nuclear receptors SF-1 and LRH-1 are constitutively active, but it remains

237 PK) converging on nuclear hormone receptors (SF-1/LRH-1) to modulate their transcriptional output.

238 ivator interactions and significantly reduce SF-1 transcriptional activity.

239 t that natural variations leading to reduced SF-1 function may underlie some forms of subclinical adr

240 at Wnt-dependent signaling cascades regulate SF-1-dependent transcription of genes required for adren

241 olipids or possibly other molecules regulate SF-1 or LRH-1 under physiological conditions.

242 olecular mechanisms by which ASAH1 regulates SF-1 function.

243 oylation may be less important in regulating SF-1 activity.

244 function, the expression of several reported SF-1 target genes, including SF-1 itself, was inhibited

245 r receptor Dax-1 binds to SF-1 and represses SF-1 target genes.

246 a novel coregulatory protein that represses SF-1 function by directly binding to the receptor on SF-

247 ce at 6-weeks were much reduced; however, SC-SF-1(-/-) seminal vesicles weights were comparable sugge

248 cell and germ cell population declined in SC-SF-1(-/-) mice resulting in the disruption of seminifero

249 ated Sertoli cell-specific Nr5a1 KO mice (SC-SF-1(-/-)) at E14.5, which coincides with testis develop

250 Analysis of SC-SF-1(-/-) (Sertoli cell specific Nr5a1 knockout) testes

251 oli and germ cells, the testis weights of SC-SF-1(-/-) mice at 6-weeks were much reduced; however, SC

252 Further analysis revealed that SC-SF-1(-/-) gonads displayed lower MDM2 levels resulting i

253 of cyclin D2, inhibin-alpha, aromatase, SCC, SF-1, and epiregulin.

254 T) was used to identify potent and selective SF-1 inverse agonists through the screening of a chemica

255 Similarly, SF-1 was also detected in the epidermis but displayed a

256 Furthermore, VMH-specific SF-1 KO mice showed significantly decreased LepR express

257 we generated pre- and postnatal VMH-specific SF-1 KO mice.

258 Both models of VMH-specific SF-1 KO were susceptible to high fat diet-induced obesit

259 coregulator recruitment of fully sumoylated SF-1 LBD protein was either unchanged or modestly impair

260 f the DEAD-box protein DP103 with sumoylated SF-1.

261 ASAH1 suppresses SF-1 activity by directly interacting with the receptor.

262 dogenic genes, without affecting synergistic SF-1 and sex-determining region Y (SRY) coactivation of

263 These findings provide evidence that SF-1 is regulated by endogenous ligands and suggest an u

264 Together, our data provide evidence that SF-1 is required for spleen development in humans via tr

265 We found that SF-1 is selectively SUMOylated at K194 in Y1 adrenocarci

266 Given that SF-1 is a nuclear protein, we sought to define the molec

267 Collectively, these results indicate that SF-1 directs transcriptional programs in the hypothalamu

268 Here we show that SF-1 +/- mice exhibit adrenal insufficiency resulting fr

269 inverse agonist lead, was used to show that SF-1 constitutive activity can be pharmacologically modu

270 these findings, cellular assays showed that SF-1 is able to activate exon I and IV promoters.

271 oximal LHbeta gene promoter and suggest that SF-1 and Egr-1 act synergistically to increase expressio

272 newborn SF-1 knockout mice, suggesting that SF-1 is essential for the development of VMH neurons.

273 structure-function relationships across the SF-1/LRH-1 subfamily indicates that ligand binding is th

274 Ishikawa cell proliferation, and induce the SF-1 target gene aromatase in a GPR30-dependent manner.

275 Further, introduction of a mutation into the SF-1 A-box, which has been proposed to bind to the 5'-fl

276 e the 1.5 angstroms crystal structure of the SF-1 ligand binding domain in complex with an LXXLL moti

277 Mutations designed to reduce the size of the SF-1 pocket or to disrupt hydrogen bonds with the phosph

278 30 and Ser-203) on SF-1 had no effect on the SF-1-dependent FUER stimulation in Y-1 and 10T1/2 cells.

279 ro transfection studies, DAX-1 repressed the SF-1-mediated transactivation of the Cyp19 promoter but

280 an LBD helix assembly assay suggest that the SF-1 LBD adopts an active conformation, with helices 1 a

281 op is topologically distinct relative to the SF-1 enzymes, both loops map to similar tertiary structu

282 ed in undifferentiated ES cells, can bind to SF-1 response elements in the proximal promoter and prox

283 pical orphan nuclear receptor Dax-1 binds to SF-1 and represses SF-1 target genes.

284 hese modifications interact or contribute to SF-1 regulation of endogenous genes remains poorly defin

285 ult, the K119R mutant, compared to wild-type SF-1, was selectively recruited to a "SUMO-sensitive" si

286 Furthermore, unsumoylatable SF-1 mutants activated Shh and exhibited preferential re

287 SAH1 is recruited to the promoter of various SF-1 target genes and that ASAH1 and SF-1 colocalize on

288 de transcriptional regulators such as Vgll2, SF-1, Sox14, Satb2, Fezf1, Dax1, Nkx2-2, and COUP-TFII,

289 to the identification of 445 gene loci where SF-1-binding regions were located from 10 kb upstream to

290 Notably, whereas SF-1 SUMOylation is independent of S203 phosphorylation

291 e an important additional mechanism by which SF-1 exerts its actions in the adrenal gland.

292 important consequences to diseases in which SF-1 activity is critical.

293 SHP is coexpressed with SF-1 in adrenal glands, but is also expressed in tissues

294 T2 cells and are capable of interacting with SF-1, GnRH stimulation of Egr-1 was the most robust.

295 ost likely through a direct interaction with SF-1.

296 also termed Gemin3 and DDX20) interacts with SF-1, SMN, EBNA2, and EBNA3C in mammalian cells.

297 inal region of DP103 directly interacts with SF-1.

298 ke induced by the complexation of STAT3 with SF-1-066 or BP-1-102 under physiological conditions enab

299 hift assays and co-transfection studies with SF-1 produced in vitro indicate F2 and F3 bind SF-1; BLA

300 1 -KTS isoforms associate and synergize with SF-1 to promote MIS expression.

301 emonstrate that beta-catenin synergizes with SF-1 to activate the alpha-inhibin promoter through form