ライフサイエンスコーパス: SRC-1

1 SRC-1 can also stimulate AF-1 activity through a seconda

2 SRC-1 does not require its bHLH-PAS domain to interact w

3 SRC-1 expression in breast cancer is associated with HER

4 SRC-1 is colocalized with apoA-IV in the cells of the NT

5 SRC-1 knockdown in human breast cancer cells also decrea

6 SRC-1 knockdown in WT cells reduced Twist expression, wh

7 SRC-1 localization experiments show that SRC-1 is reloca

8 SRC-1 may promote metastasis through mediating Ets-2-med

9 SRC-1 was required for the aggressive and motile phenoty

10 SRC-1(-/-)/PyMT mammary tumors were also more differenti

11 SRC-1, SRC-2, and SRC-3 all enhanced IkappaB alpha trans

12 o increased steroid receptor co-activator 1 (SRC-1) interaction with the PR NTD and cooperated with S

13 (PCAF) and steroid receptor co-activator 1 (SRC-1), the full length ACTN4 protein either does not or

14 ns with the steroid receptor co-activator-1 (SRC-1) peptide, displacing SRC-1 binding.

15 cannot bind steroid receptor coactivator 1 (SRC-1) and Src-1(-/-) mice both have phenotypes similar

16 cruitment of steroid receptor coactivator 1 (SRC-1) and subsequent histone H4 acetylation at the targ

17 teracts with steroid receptor coactivator 1 (SRC-1) and that UBCH7 coactivation function is dependent

18 CBP/p300 and steroid receptor coactivator 1 (SRC-1) and the p300/CBP-associated factor (P/CAF) for op

19 igh level of steroid receptor coactivator 1 (SRC-1) expression.

20 protein, and steroid receptor coactivator 1 (SRC-1) in cell transfection and immunoprecipitation stud

21 ctivation by steroid receptor coactivator 1 (SRC-1) of mCAR did not depend on the threonine 350.

22 e to trigger steroid receptor coactivator 1 (SRC-1) recruitment and histone H3 acetylation.

23 protein with steroid receptor coactivator 1 (SRC-1), an essential component of steroid hormone signal

24 n of GR with steroid receptor coactivator 1 (SRC-1).

25 Steroid receptor coactivator-1 (SRC-1 or NCOA1) is overexpressed in a subset of breast c

26 ivators, the steroid receptor coactivator-1 (SRC-1) and the peroxisome proliferator-activated recepto

27 of the human steroid receptor coactivator-1 (SRC-1) containing one LXXLL motif.

28 east cancer, steroid receptor coactivator-1 (SRC-1) expression positively correlates with HER2 expres

29 Steroid receptor coactivator-1 (SRC-1) is a coactivator for nuclear hormone receptors su

30 mplex is the steroid receptor coactivator-1 (SRC-1) which interacts with the receptor complex via spe

31 n-1(GRIP-1)/steroid-receptors coactivator-1 (SRC-1)) without breaking it.

32 Steroid receptor coactivator-1 (SRC-1), a coregulatory protein of the oestrogen receptor

33 tors such as steroid receptor coactivator-1 (SRC-1), RU486-bound PR binds to both coactivator SRC-1 a

34 discovery of steroid receptor coactivator-1 (SRC-1), the first authentic coregulator, more than 400 c

35 ors, such as steroid receptor coactivator-1 (SRC-1), to facilitate the transcription of targeted gene

36 sly for steroid receptor coactivator type 1 (SRC-1) and SRC-3 female knockout mice.

37 etrically localized in response to the MES-1/SRC-1 signaling pathway.

38 that steroid receptor coactivators 1 and 2 (SRC-1 and SRC-2) regulate surfactant protein-A (SP-A) an

39 on of steroid receptor coactivators 1 and 2 (SRC-1 and SRC-2), which upregulate SP-A transcription, t

40 t, pro-adipogenic roles for SRC-2 and SRC-3, SRC-1 knockdown does not affect adipogenesis.

41 d SRC-1 with SI-2, a second-generation SRC-3/SRC-1 small-molecule inhibitor, targets the CSC/TIC popu

42 ERE together with histone acetyltransferases SRC-1 and p300, ubiquitin ligase E6-AP, histone methyltr

43 Co-transfection of the co-activator, SRC-1, further slowed the mobility of liganded GFP-ER.

44 SKIP entering these promoter complexes after SRC-1.

45 Although SRC-1 concentrates in Sertoli cell nuclei in the absence

46 An SRC-1-null mouse model reveals that the mouse SRC-1 gene

47 ity group box 2 (HMGB2) was identified as an SRC-1 interacting protein in the endocrine-resistant set

48 the p160 family of co-activators GRIP-1 and SRC-1 in a two-hybrid assay.

49 We also show that inhibition of SRC-3 and SRC-1 with SI-2, a second-generation SRC-3/SRC-1 small-m

50 otent small-molecule inhibitor for SRC-3 and SRC-1.

51 esence of AR coregulators, such as ARA70 and SRC-1.

52 ators p300, CREB-binding protein, p/CIP, and SRC-1.

53 ment enhances the recruitment of ERalpha and SRC-1 to the estrogen response element at the apoA-V pro

54 ne the functional interaction between GR and SRC-1 and further define the role of the GR in glucocort

55 n studies reveal that the SR12813 ligand and SRC-1 coactivator peptide each stabilize the LBD of PXR,

56 crine-resistant breast cancer cell lines and SRC-1(-/-)/PyMT mice confirmed a role for SRC-1 and HOXC

57 require a critical balance between NCoR1 and SRC-1.

58 T(3) sensitivity in the absence of NCoR1 and SRC-1.

59 n with transcription co-regulators NCoR1 and SRC-1.

60 ors and coactivators, including CBP/p300 and SRC-1.

61 he histone acetyltransferases CBP, p300, and SRC-1 in a hormoneindependent manner, an association not

62 HPV-16 E6 to compete with NF-kappaB/p65 and SRC-1 for binding to the N terminus and C terminus of CB

63 e histone acetyltransferases (HATs) PCAF and SRC-1 form a complex with both H4R3 histone methyltransf

64 Since Mig-6 is regulated by both PR and SRC-1, this identifies a PR, SRC-1, Mig-6 regulatory pat

65 ein but independent of coactivators PRIP and SRC-1.

66 astatic analysis of transplanted WT/PyMT and SRC-1(-/-)/PyMT tumors in SRC-1(-/-) and WT recipient mi

67 background, thus demonstrating that TIF2 and SRC-1 can perform redundant functions in Sertoli cells.

68 ies in molecular pathways involving TIF2 and SRC-1 in Sertoli cells could participate in testicular s

69 We now report that constructs of TIF2 and SRC-1 lacking the two activation domains (AD1 and AD2) h

70 Coactivators such as TIF2 and SRC-1 modulate the positioning of the dose-response curv

71 STAMP associates with coactivators (TIF2 and SRC-1) and is selective for a subset of the steroid/nucl

72 es displayed by the SRC-1(+/-)/TIF2(-/-) and SRC-1(-/-)/TIF2(-/-) mutant testes, including spermatid

73 n-regulates SRC-1-mediated transcription and SRC-1-associated HAT activity.

74 Furthermore, injection of anti-SRC-1 or anti-p/CIP immunoglobulin G into mammalian cell

75 tion (ChIP) assays showed recruitment of AR, SRC-1, Med-1, transcription factor IIB (TFIIB), and poly

76 ator 1 and 3 (NCOA1 and NCOA3, also known as SRC-1 and SRC-3) to an AR-ROR response element (RORE) to

77 activating them indirectly through augmented SRC-1 coactivation.

78 stations also occurred in WT females bearing SRC-1/-2 double-deficient embryos, indicating that a fet

79 there was a significant association between SRC-1 and Ets2 in the recurrent tissue compared with the

80 the hormone-independent association between SRC-1 and X-RARalpha on the array has been identified.

81 tudies revealed that the interaction between SRC-1 and PR is dependent upon phosphorylation of SRC-1.

82 ic progression in which interactions between SRC-1 and Ets2 promote dedifferentiation and migration i

83 Direct interactions between SRC-1 and the transcription factor Ets2 regulated Myc an

84 Both SRC-1 and SMRT have the capacity to modulate RU486-depen

85 Both SRC-1 and TIF2 are members of the p160 steroid receptor

86 T dams crossed with males deficient for both SRC-1 and SRC-2 had suppressed myometrial inflammation,

87 As mice lacking both SRC-1 and SRC-2 die at birth due to respiratory distress

88 to the transcriptional initiation site; both SRC-1 and c-Jun were recruited to this promoter region i

89 In the adult mouse brain, SRC-1 is highly expressed in the olfactory bulb, hippoca

90 ediately, suggesting replacement of SRC-2 by SRC-1.

91 minal interaction and was not coactivated by SRC-1.

92 bryo implantation, a phenotype not shared by SRC-1 or -3 knockout mice.

93 vators or coactivator-binding proteins (CBP, SRC-1, PBP, PRIP, PIMT, TRAP100, SUR-2, and PGC-1), othe

94 1), RU486-bound PR binds to both coactivator SRC-1 and corepressor silencing mediator for retinoid an

95 ved motif (B-box) with mammalian coactivator SRC-1, and we establish that B-box is a critical determi

96 full-length ERalpha or the p160 coactivator SRC-1.

97 he role of the androgen receptor coactivator SRC-1 in prostate cancer progression.

98 pression of the steroid receptor coactivator SRC-1.

99 r, promotes interaction with the coactivator SRC-1, and efficiently activates PPARbeta/delta-mediated

100 One of these is the coactivator SRC-1, whose binding to PR and enhancement of agonist-de

101 cruitment of the transcriptional coactivator SRC-1 both in vitro and in vivo.

102 ional activity by competing with coactivator SRC-1.

103 eptor (PR) and steroid receptor coactivator (SRC-1) action in the uterus.

104 th PXR and the steroid receptor coactivator (SRC-1) were found to bind to PXREs in the absence of rif

105 creases recruitment of the p160 coactivators SRC-1 and GRIP1.

106 ng interaction with RXR and the coactivators SRC-1 and DRIP205.

107 ptor interaction domains of the coactivators SRC-1 and GRIP1.

108 RNA polymerase II, PR, and the coactivators SRC-1 and SRC-2 to the distal region and basal promoter.

109 we investigated recruitment of coactivators (SRC-1, SRC-2, and SRC-3) and corepressors (HDAC1, HDAC2,

110 augments the activity of p160 coactivators (SRC-1 and TIF2) in glucocorticoid receptor-regulated gen

111 r cells rely, steroid receptor coactivators (SRC-1, SRC-2, and SRC-3) represent emerging targets in c

112 160 family of steroid receptor coactivators (SRC-1, SRC-2, and SRC-3) steer the functional output of

113 ificantly reduced mRNA for the coactivators, SRC-1 (42%, P<0.01) and 2 (47%, P<0.03), and diminished

114 Combined SRC-1 and HOXC11 ChIPseq analysis identified the differe

115 We confirmed SRC-1 as a regulator of ADAM22 by molecular, cellular, a

116 In contrast, SRC-1 was involved in the down-regulation of PR target g

117 lpha bind to the transcriptional coregulator SRC-1 with higher affinity when they are part of the PXR

118 During embryonic development, SRC-1 is expressed in the cerebellar primordium.

119 , and the apoptotic protein, PAWR, as direct SRC-1/HOXC11 suppression targets.

120 r co-activator-1 (SRC-1) peptide, displacing SRC-1 binding.

121 fen (4HT) and raloxifene are able to elevate SRC-1 and SRC-3 protein levels.

122 nd suggest that reduced levels of endogenous SRC-1 and apoA-IV expression are responsible for the imp

123 ociated with the recruitment of liganded ER, SRC-1, p300, ubiquitin ligase E6-AP (E6L), Mdm2, and pol

124 h, IGF-1 increased the recruitment of the ER.SRC-1.p300.E6L.Mdm2.Carm.pol II complex on AP-1, but not

125 RC-2, and partially prevented with exogenous SRC-1.

126 Purkinje cells (PCs) preferentially express SRC-1 over SRC-2, but SRC-2 mRNA is slightly elevated in

127 e steroid receptor coactivator (SRC) family, SRC-1, TIF2/GRIP1/SRC-2, and pCIP/ACTR/AIB-1/RAC-3/TRAM-

128 This contact is essential for SRC-1 recruitment and subsequent dexamethasone-induced G

129 nd SRC-1(-/-)/PyMT mice confirmed a role for SRC-1 and HOXC11 in downregulation of CD24 and PAWR.

130 k down assays revealed an important role for SRC-1.

131 A peptide derived from SRC-1 RID2 is used to study the thermodynamic properties

132 gand and a coactivator sequence derived from SRC-1.

133 Furthermore, SRC-1 was found to coactivate Twist transcription throug

134 Furthermore, SRC-1 was up-regulated during mammary tumor progression.

135 Furthermore, SRC-1, NCoA-2, and p/CIP all associate with the CYP1A1 e

136 The p160 coactivators (e.g., SRC-1, GRIP1, and ACTR) bind directly to activated NR an

137 complex includes a p160 coactivator (GRIP1, SRC-1, or ACTR) and its downstream coactivators (e.g., p

138 ex includes a p160 coactivator (e.g., GRIP1, SRC-1, or ACTR) that binds directly to activated NR, the

139 d (~38 hours) in heterozygous dams harboring SRC-1/-2-deficient embryos.

140 In the resistant setting, the HMGB2, SRC-1 and ER complex are enriched at promoter regions of

141 Our findings deepen the understanding of how SRC-1 controls transcription in breast cancers.

142 n in the NTS was significantly attenuated in SRC-1 knockdown rats.

143 A further delay in SRC-1(-)/- PC maturation was detected at the neonatal st

144 In addition, no significant difference in SRC-1, p300, or TIP60 expression was found.

145 notypes of brain development and function in SRC-1 knock-out (SRC-1(-)/-) mice.

146 breast cancer cells or knockdown of ITGA5 in SRC-1-expressing breast cancer cells was associated with

147 Therefore, targeting ITGA5 in SRC-1-positive breast cancers may result in inhibition o

148 niferous epithelial degeneration observed in SRC-1(+/-)/TIF2(-/-) testes.

149 teolysis, and rescued delayed parturition in SRC-1/-2-deficient embryo-bearing dams.

150 lung metastasis were drastically reduced in SRC-1(-/-)/PyMT mice compared with WT/PyMT mice.

151 vating factor (PAF) were markedly reduced in SRC-1/-2-deficient fetal lungs near term.

152 Furthermore, ITGA5 reduction in SRC-1-deficient/insufficient breast cancer cells or knoc

153 tumor initiation and growth were similar in SRC-1(-/-)/PyMT and wild-type (WT)/PyMT mice, genetic ab

154 lanted WT/PyMT and SRC-1(-/-)/PyMT tumors in SRC-1(-/-) and WT recipient mice revealed that SRC-1 pla

155 d ERbeta, and formed a complex that included SRC-1, but not CBP, N-CoR or SMRT.

156 uclear receptor coactivators, which includes SRC-1 (NCoA-1) and SRC-2 (TIF2/GRIP1/NCoA2).

157 RC-1 protein levels, we found that increased SRC-1 expression in clinically localized, androgen-depen

158 However, mutation of the two cAMP-inducible SRC-1 phosphorylation sites important for cAMP activatio

159 Interestingly, SRC-1 appears to negatively influence AR activity, there

160 Interestingly, SRC-1 expression in primary and/or recurrent tumors was

161 Interestingly, SRC-1 gene expression is significantly reduced in DIO OV

162 full-length SRC-1, the endometriotic 70-kDa SRC-1 C-terminal fragment prevents TNF-alpha-mediated ap

163 9) activity mediates formation of the 70-kDa SRC-1 C-terminal isoform in endometriotic mouse tissue.

164 Notably, a previously unidentified 70-kDa SRC-1 proteolytic isoform is highly elevated both in the

165 ken progesterone receptor or all seven known SRC-1 phosphorylation sites did not specifically impair

166 In contrast to full-length SRC-1, the endometriotic 70-kDa SRC-1 C-terminal fragmen

167 nctional interventions for coactivators like SRC-1 may provide unique approaches to control breast ca

168 n signaling pathways and in which localizing SRC-1 activity to UNC-5 is crucial for proper signal tra

169 Using tissue arrays to measure SRC-1 protein levels, we found that increased SRC-1 expr

170 analyses of SRC-1/TIF2 compound mutant mice, SRC-1 can partially compensate for the effects of a loss

171 ctively, the newly identified TNF-alpha-MMP9-SRC-1 isoform functional axis promotes pathogenic progre

172 a middle T (PyMT) breast cancer mouse model, SRC-1 strongly promotes mammary tumor metastasis.

173 RC-1-null mouse model reveals that the mouse SRC-1 gene has an essential role in endometriosis progre

174 lly, overexpression of GRIP-1/TIF-2, but not SRC-1, potentiates ROR(alpha)-stimulated Reverb(alpha) p

175 ave shown that inactivation of TIF2, but not SRC-1, reduces postnatal survival, growth, and male repr

176 tively demonstrate the critical roles of NTS SRC-1 in mediating E2's actions on food intake and apoA-

177 cell nuclei in the absence of TIF2, nuclear SRC-1 is not able to rescue AR activity in the TIF2 muta

178 that it involves the differential ability of SRC-1 to modulate expression levels of distinct coactiva

179 ild-type (WT)/PyMT mice, genetic ablation of SRC-1 antagonized PyMT-induced restriction of mammary du

180 Although absence of SRC-1 prevented T(3) activation of key hepatic gene targ

181 sion attenuates the coactivating activity of SRC-1, suggesting that exchange between TTP and other co

182 also requires the intact kinase activity of SRC-1.

183 re, we demonstrate that, through analyses of SRC-1/TIF2 compound mutant mice, SRC-1 can partially com

184 Here, we report that a global analysis of SRC-1 target genes suggested that SRC-1 also mediates tr

185 rved thermodynamic parameters for binding of SRC-1 peptide to liganded and apo CAR-RXR as well as the

186 of residues that are involved in binding of SRC-1 to PXR.

187 eceptor coactivator (SRC) family composed of SRC-1 (NCOA1), SRC-2 (TIF2/GRIP1/NCOA2), and SRC-3 (AIB1

188 To test the contribution of SRC-1, we examined its role in androgen-dependent LNCaP

189 analyzed the cell-specific contributions of SRC-1 and TIF2 to the activity of AR in mouse testis.

190 rmed by using cells individually depleted of SRC-1, SRC-2, or SRC-3 by small interfering RNA.

191 Disruption of SRC-1 also suppressed colony-stimulating factor-1 (CSF-1

192 Disruption of SRC-1 inhibited Ets-2-mediated HER2 expression and PyMT-

193 Disruption of SRC-1 specifically delays the PC development and maturat

194 CAR3 with the receptor interaction domain of SRC-1, indicating that RXR augments CAR3 activity by fac

195 main of UNC-5 and an intracellular domain of SRC-1.

196 Dysregulation of SRC-1 localization and function by HPV E7 may provide in

197 to be due, in part, to reduced expression of SRC-1 and -2, which is a novel mechanism by which inflam

198 erestingly, there was variable expression of SRC-1 in normal prostate tissue which correlated with th

199 ptor activity through elevated expression of SRC-1 in the development of more aggressive disease in m

200 s uniformly accelerated upon inactivation of SRC-1 alleles in the TIF2 null genetic background, thus

201 han SRC-1 and stimulates AF-1 independent of SRC-1 pathways.

202 e breast cancers may result in inhibition of SRC-1-promoted breast cancer metastasis.

203 ivity is associated with receptor instead of SRC-1 phosphorylation.

204 4 significantly increased the interaction of SRC-1 with FXR.

205 Intervention of SRC-1 function may provide new strategies to inhibit bre

206 Moreover, a change in the relative levels of SRC-1 and SMRT contained in our chromatin transcription

207 hase despite comparable expression levels of SRC-1 and SRC-3.

208 ed cells, demonstrated decreased mobility of SRC-1 on the X-RARalpha-bound chromatin.

209 The morphology and number of SRC-1(-)/- PCs were equivalent to wild type by P10; this

210 However, overexpression of SRC-1 counteracted progesterone to repress mCAR activity

211 ating concentrations, (ii) overexpression of SRC-1 led to loss of cooperativity and even to strong re

212 oA-V promoter, implying the participation of SRC-1 in E2's stimulatory effect on apoA-IV gene express

213 spatial and temporal expression patterns of SRC-1 and characterized the phenotypes of brain developm

214 and PR is dependent upon phosphorylation of SRC-1.

215 rse analysis revealed that the precursors of SRC-1(-)/- PCs were generated approximately 2 d later th

216 eceptors exhibit preferential recruitment of SRC-1 family coactivators, which determines the subseque

217 ently in the G1 and S phases, recruitment of SRC-1, SRC-3, and, consequently, CBP is reduced in G1 ph

218 Reduction of SRC-1 expression significantly reduced growth and altere

219 on by association with and relocalization of SRC-1.

220 Moreover, removal of SRC-1 in the PR(Cre/+) SRC-2(flox/flox) mouse uterus res

221 To study the role of SRC-1 in brain development and function, we examined the

222 tigen (PyMT) mice to investigate the role of SRC-1 in breast cancer.

223 gets and mechanisms that mediate the role of SRC-1 in metastasis are unknown.

224 ments further support the predicted roles of SRC-1 and SRC-2 in, respectively, PR- and GR-mediated tr

225 estrogen receptor (ER)-independent target of SRC-1.

226 UBCH7 coactivation function is dependent on SRC-1.

227 rformed to determine the effect of HPV E7 on SRC-1-associated HAT activity.

228 t of high- and low-risk HPV E7 expression on SRC-1-mediated transcription.

229 Knockdown of Med-1 and/or SRC-1 demonstrated the presence of a nonproductive compl

230 DES did not alter ER or SRC-1 binding to HOXA10 ERE1.

231 en PRMT2 was coexpressed with either PRIP or SRC-1.

232 development and function in SRC-1 knock-out (SRC-1(-)/-) mice.

233 ent kinase, retinoblastoma protein, or p160 (SRC-1) functions in human breast and prostate cancer cel

234 ed AhR and HDAC1, reduced occupancy by p300, SRC-1, and diminished acetylation of H4 at the BRCA-1 pr

235 Overexpression of p300, SRC-1 or pCAF did not abrogate AP-1 suppression by RA, t

236 ta directly and recruits coactivator peptide SRC-1.

237 In agreement with this phenotype, SRC-1 expression positively correlated with integrin alp

238 by both PR and SRC-1, this identifies a PR, SRC-1, Mig-6 regulatory pathway that is critical in the

239 Bigenic PRAI-SRC-1(-/-) mice revealed that SRC-1 modulates PR activit

240 The steroid coactivator protein SRC-1, through interactions with developmental proteins

241 nt of steroid receptor coactivator proteins (SRC-1 or -2), although SRC transfection augmented AR act

242 n a conformation able to efficiently recruit SRC-1, unless SRC-1 is overexpressed.

243 veal that HPV16 E7 expression down-regulates SRC-1-mediated transcription and SRC-1-associated HAT ac

244 The RXR ligand, 9-cis-RA, generates a second SRC-1 site and increases the affinity by improving the e

245 BP-associated factor (PCAF), members of some SRC-1 transcriptional complexes.

246 he p160 steroid receptor coactivators (SRCs) SRC-1, SRC-2 [nuclear receptor coactivator (NCOA)2], and

247 and its steroid receptor coactivators (SRCs; SRC-1, -2 and -3) were recurrently affected by these SiM

248 In this study, SRC-1 wild-type (WT) and knockout (KO) cell lines were d

249 In this study, SRC-1(-/-) mice were backcrossed with FVB mice and then

250 Substituting SRC-1 with Adnectin-1 does not alter the binding conform

251 stantially stronger coactivator of AF-1 than SRC-1 and stimulates AF-1 independent of SRC-1 pathways.

252 gnals to initiate labor when mature and that SRC-1/-2-dependent production of SP-A and PAF is crucial

253 cipitation and by a reporter gene assay that SRC-1 and NCoA-2 but not p/CIP are capable of interactin

254 In this report, we demonstrate that SRC-1, NCoA-2, and p/CIP are capable of independently en

255 Herein, we found that SRC-1 deficiency in mouse and human breast cancer cells

256 Finally, we found that SRC-1 enhanced ITGA5 promoter activity through an AP-1 (

257 ed in cultured neuronal cells, we found that SRC-1 gene knockdown specifically in the NTS significant

258 We previously reported that SRC-1 promotes breast cancer metastasis without affectin

259 Bigenic PRAI-SRC-1(-/-) mice revealed that SRC-1 modulates PR activity in the uterus in a cell-spec

260 C-1(-/-) and WT recipient mice revealed that SRC-1 played an intrinsic role in tumor cell metastasis.

261 Multiple behavioral tests revealed that SRC-1(-)/- mice exhibit normal hippocampal function but

262 These results show that SRC-1 can promote breast cancer metastasis by directly e

263 SRC-1 localization experiments show that SRC-1 is relocalized to the cytoplasm in the presence of

264 Here, we showed that SRC-1 interacts with the cytosolic domain of UNC-5 throu

265 These results suggest that SRC-1 specifically promotes metastasis without affecting

266 Taken together, our findings suggest that SRC-1 switches steroid-responsive tumors to a steroid-re

267 nalysis of SRC-1 target genes suggested that SRC-1 also mediates transcriptional repression in breast

268 The SRC-1 peptide forms two distinct helices and binds adjac

269 The SRC-1/NCoA-1, NCoA-2/GRIP-1/TIF-2, and p/CIP/AIB/ACTR pr

270 e overall abnormal features displayed by the SRC-1(+/-)/TIF2(-/-) and SRC-1(-/-)/TIF2(-/-) mutant tes

271 ed with the early expression of SRC-2 in the SRC-1(-)/- PCs.

272 , but SRC-2 mRNA is slightly elevated in the SRC-1(-)/- PCs.

273 ose with the TIF2+/- mutation but not in the SRC-1+/- background, suggesting that TIF2 serves as the

274 1 in not only targeting the interface of the SRC-1 interactions but also engaging the same set of res

275 MD2C/KDM4C), respectively, as members of the SRC-1 interactome responsible for transcriptional repres

276 ement in the CXCR4 promoter and recruits the SRC-1-p300 complex to promote H4K5 and H4K16 histone ace

277 rs to a steroid-resistant state in which the SRC-1 target gene ADAM22 has a critical role, suggesting

278 lutamide-liganded AR could interact with the SRC-1 glutamine-rich domain that mediates AR NH(2)-termi

279 ssay shows TTF-1 direct interaction with the SRC-1 histone acetyltransferase domain.

280 crossing AR activity indicator mice with the SRC-1-/- or TIF2+/- mutant mice.

281 Therefore, SRC-1 promotes breast cancer invasiveness and metastasis

282 Increased transcription due to SRC-1 is independent of PR SUMOylation based on assays w

283 After tumor necrosis factor-alpha treatment, SRC-1 signal was increased gradually, but SRC-2 signal w

284 on able to efficiently recruit SRC-1, unless SRC-1 is overexpressed.

285 cyclic pattern of promoter occupancy by VDR, SRC-1, and NCoA62/SKIP was observed, with NCoA62/SKIP en

286 In most brain structures where SRC-1 is expressed, SRC-2 is expressed at lower levels;

287 n WT cells reduced Twist expression, whereas SRC-1 restoration in KO cells also rescued Twist express

288 f TIF2 on mouse survival and growth, whereas SRC-1 and TIF2 are dispensable for primary organogenesis

289 ogen receptor-negative breast tumors whereas SRC-1 deficiency decreased ITGA5 expression.

290 Finally, we dissected the means by which SRC-1 dynamically regulates PR activity in each uterine

291 Our results support a model in which SRC-1 is required for UNC-5-induced axon repulsion and g

292 onfirm the interactions of ARNT and AHR with SRC-1 with immunocytochemical techniques.

293 al cells facilitated interactions of AR with SRC-1 in an androgen-dependent manner.

294 eraction with the PR NTD and cooperated with SRC-1 to stimulate NTD-dependent transcriptional activit

295 absence of synergism by PCAF or DRIP150 with SRC-1 or TIF2, respectively, further suggests that these

296 its transactivation domain to interact with SRC-1.

297 AF1 is well-suited for its interaction with SRC-1.

298 oactivators, CBP, p300, and PBP but not with SRC-1 and PGC-1alpha under in vitro and in vivo conditio

299 receptor (PR) interacted preferentially with SRC-1, which recruited CBP and significantly enhanced ac

300 PV16 E7 associates in vivo and in vitro with SRC-1 independently of p300 and PCAF.