ライフサイエンスコーパス: E2F4

1 ciated earlier with mutation of either Rb or E2f4.

2 oters were bound by E2F6, but not by E2F1 or E2F4.

3 ted with increased cytosolic localization of E2F4.

4 ranscriptionally regulated, in part, by p130:E2F4.

5 ction of the C-terminal Rb binding region of E2F4.

6 n B1 and decreased levels of CDK2, CDK4, and E2F4.

7 E2F1 and was not observed in E2F2, E2F3, or E2F4.

8 ic translocation of the transcription factor E2f4.

9 p130 and the inhibitory transcription factor E2F4.

10 sence of either E2F2 or E2F3 but not E2F1 or E2F4.

11 o role of the predominant E2F family member, E2F4.

12 amatic increase in the level of E2F1 but not E2F4.

13 onstrated that Trim28 can bind both E2F3 and E2F4.

14 the cytoplasmic-to-nuclear translocation of E2F4.

15 ir-17, suggestive of regulation of miRNAs by E2F4.

16 effect was blocked by a cDNA expressing the E2F4 3'-UTR sense strand.

17 that both beta-catenin and TCF4 bind to the E2F4 3'-UTR site in vivo, inducing expression of an E2F4

18 as growth-restraining members of the family (E2F4, -5, and -6) have little effect.

19 containing Smad3, the transcription factors E2F4/5 and DP1, and the corepressor p107 preexists in th

20 timate recipients of cdk regulatory signals, E2F4/5 and p107 act here as transducers of TGFbeta recep

21 cence through scaffolding MuvB proteins with E2F4/5 and the Rb tumor suppressor paralog p107 or p130.

22 As E2F4/5 are essential downstream mediators for a p16INK4a

23 sting of a Smad-binding site and an adjacent E2F4/5 element, structurally similar to the TIE found on

24 1 also blocks the function of E2F4 and E2F5 (E2F4/5) transcription factors through promoting their nu

25 of TGF-beta by forming a complex with Smad3, E2F4/5, and p107 at the TGF-beta inhibitory element (TIE

26 occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SU

27 130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a lin

28 ily proteins that transcriptionally activate E2F4/5-target genes during multiciliogenesis, including

29 tion of transcription at G1/S and a role for E2F4-8 in repressing the same group of E2F1-3 target gen

30 quired for Schwann cell differentiation, and E2F4, a cell cycle regulator, showed a strong requiremen

31 ese observations suggest a critical role for E2F4 activity in controlling the maturation of cells in

32 To study the effect of deregulated E2F4 activity on cell growth control and tumorigenesis,

33 We have generated mice deficient in E2F4 activity, the major form of E2F in many cell types.

34 y and its binding partner DP-1 revealed that E2F4 acts as an activator as well as a repressor.

35 In these cells, E2F4 acts in part as a transcriptional activator that pr

36 In this study, we analyse how loss of E2f4 affects the tumorigenicity of pRB-deficient tissues

37 This analysis shows that loss of E2F4 allows cells to undergo spontaneous differentiation

38 We focused on whether E2F4, an E2F member believed to exhibit crucial control

39 creased levels of cell cycle genes including E2f4 and Ccne1 as early as 6 h following Etv2 induction.

40 Further characterization of the role of E2F4 and Daxx as well as other differentially expressed

41 and led to the release of p130 and MuvB from E2F4 and decreased p130 and MuvB binding to cell cycle p

42 E2F4 and DP2 interact through an extensive protein-prote

43 strate that LMP1 also blocks the function of E2F4 and E2F5 (E2F4/5) transcription factors through pro

44 Thus, E2F4 and E2F5 are dispensable for cell cycle progression

45 E2F4 and E2F5 constitute a defined subset of the family.

46 ly reflects the control of expression of the E2F4 and E2F5 genes.

47 we report that simultaneous inactivation of E2F4 and E2F5 in mice results in neonatal lethality, sug

48 g a supershift with the antibody against the E2F4 and E2F5 pocket protein, p107.

49 But, unlike the E2F4 and E2F5 proteins, which are also expressed in quie

50 ifferentially with the cell-cycle regulators E2F4 and E2F5, which enables them to activate distinct s

51 7 and p130 almost exclusively associate with E2F4 and E2F5.

52 Indeed, inhibition of both E2F4 and E2F6 activity results in specific derepression

53 ate corepressor complexes consisting of p130-E2F4 and HDAC1/2-mSin3B from the promoters of E2F-regula

54 ysis provided evidence of versatile roles of E2F4 and insights into its functions.

55 trated that both the nuclear localization of E2F4 and its association with the Rb family member p130

56 Overexpression of E2F4 and its transcriptional cofactors of the retinoblas

57 protein (RB) and DREAM complex (DP, RB-like, E2F4 and MuvB) cooperate to repress all cell cycle genes

58 s involves the DREAM complex (DP, p130/RBL2, E2F4 and MuvB), a newly identified key regulator of quie

59 ining p107 and enhances its interaction with E2F4 and other p107 partners.

60 )/early G(1), Mip/LIN-9 forms a complex with E2F4 and p107 or p130, while in late G(1)/S phase, it as

61 F4/p130 complexes and increased occupancy of E2F4 and p130 at the RAD51 and BRCA1 promoters.

62 t bound an inhibitory E2F complex containing E2F4 and p130.

63 Loss of E-cadherin activates the E2F4 and p130/107 transcription repressor complexes to s

64 We find that E2F4 and pocket protein association with the Plk1 promot

65 gulation of pocket protein interactions with E2F4 and the expression of p107 and E2F1, both E2F-regul

66 cell cycle regulatory transcription factors E2F4 and the MAGE protein necdin were similarly altered

67 growth and may involve interactions between E2F4 and the neuronal differentiation program itself.

68 lex, together with the Rb-like protein p130, E2F4, and DP1, forms the DREAM complex during quiescence

69 minimally affects the binding of E2F2, E2F3, E2F4, and E2F5 but significantly inhibits the binding of

70 We determined that most E2F1, E2F4, and E2F6 binding sites are located within 2 kb of

71 Second, it is a specific property of E2F4, and not other E2Fs, and it occurs independently of

72 F-beta increases the nuclear localization of E2F4, and presumably the transcriptional repression of t

73 ner for repression of pro-apoptotic genes is E2F4, and that the p130-E2F4 complex recruits the chroma

74 onal suppression involving Smads 2 and 3, Rb/E2F4, and the cell-cycle repressor elements CDE and CHR.

75 nding activity, composed largely of E2F2 and E2F4, and the growth-suppressive E2F4-p130 complexes.

76 nt signaling, also induced expression of the E2F4 antisense transcript and decreased E2F4 protein lev

77 -UTR site in vivo, inducing expression of an E2F4 antisense transcript.

78 egulated the in vivo transition from E2F3 to E2F4 as the major E2F DNA binding activity, and its cont

79 ase in E2F4 protein was reflected by reduced E2F4 association with specific target genes, including C

80 are lost rapidly along with the presence of E2F4 at E2F-containing B-Myb promoter sites.

81 Chromatin immunoprecipitation localized E2F4 at promoter regions of the Bub3 and Pttg1 mitotic g

82 The switch between E2F1 and E2F4 at the E2F binding site of the cyclin B1 promoter c

83 the occupancy of the transcription repressor E2F4 at the EZH2 promoter following PARP inhibition.

84 reduced expression of E2F1 and E2F2, but not E2F4, at the mRNA and protein levels.

85 regulated by Sp1 and negatively regulated by E2F4-based transcriptional complexes.

86 data suggest that in response to radiation, E2F4 becomes active in the nucleus, enforces a stable G(

87 While half of all E2F4 binding sites (56%) occurred near transcription sta

88 E2F4 binding sites also occurred near regulatory element

89 uencing (ChIP-seq) to identify around 16,000 E2F4 binding sites which potentially regulate 7346 downs

90 was accompanied by decreased p130, p107, and E2F4 binding to Cdk2.

91 ncrease of E2F4 levels led to an increase in E2F4 binding to p130 but had no effect on E2F4/p107 or E

92 cting E2F site in the cdc2 promoter, whereas E2F4 binds to the negative-acting site.

93 ound to the activator site and both E2F1 and E2F4 bound to the repressor site of the Rb promoter in v

94 ate that BRG1 binds specifically to E2F6 and E2F4 but not the activator E2Fs.

95 Individual export mutants of E2F4, but not a mutant with inactivation of both export

96 ssed in keratinocytes transgenic for E2F1 or E2F4, but not in c-myc transgenics.

97 bunit protein complex that contains p130 and E2F4, but not pRB, and mediates the repression of cell c

98 r, inactivation of Rb or substitution of the E2F4 C-terminal domain by the E2F1 C-terminal region res

99 In the absence of E2F6, E2F4 can bind to the G1/S-regulated promoters and compen

100 er, other members of the E2F family (such as E2F4) cannot.

101 carcinogenesis by reducing the level of the E2F4 cell cycle repressor via an antisense mechanism.

102 Moreover, a subset of the Rb(-/-);E2f4(-/-) chimeras developed either low- or high-grade c

103 ssion increased the longevity of the Rb(-/-);E2f4(-/-) chimeric animals allowing us to identify novel

104 line mice die in utero, we generated Rb(-/-);E2f4(-/-) chimeric animals to allow examination of adult

105 Following radiation treatment, E2F4 colocalized with p130 in the nucleus during a radia

106 through small interfering RNA prevented p130/E2F4 complex formation and sensitized cells to IR-induce

107 The C/EBPalpha-Rb-E2F4 complex occupies the c-myc promoter and blocks indu

108 o-apoptotic genes is E2F4, and that the p130-E2F4 complex recruits the chromatin modifiers HDAC1 and

109 We identified an age-specific C/EBPalpha-Rb-E2F4 complex that binds to E2F-dependent promoters and r

110 y the transcriptional repression of the p130:E2F4 complex.

111 xpression and a shift to an active repressor E2F4 complex.

112 roteins and the release of p130 and pRB from E2F4 complexes allows formation of E2F1 complexes not on

113 mal growth-arrested enterocytes contain p130-E2F4 complexes and that T-antigen expression destroys th

114 in response to either p53 or p21 induction, E2F4 complexes are specifically recruited onto the promo

115 not with p53 activation targets, implicating E2F4 complexes as effectors of p21-dependent p53-mediate

116 nally, amounts of p27-cyclin E and RB-2/p130-E2F4 complexes were found to increase in CA-OV3 cells gr

117 romoters by repressive PRC1.6/E2F6 and DREAM/E2F4 complexes.

118 30 and p107 as well as the formation of p107-E2F4 complexes.

119 lation in the nucleus, and formation of RBL2/E2F4 complexes.

120 Taken together, our data show that pRB and E2F4 cooperate in placental development, but play largel

121 We found that p130 and E2F4 cooperatively repress a common set of genes under e

122 We analyzed the impact of E2F4 deficiency on early steps in mouse hematopoietic de

123 Here we establish that E2f4 deficiency reduced the lifespan of Rb(-/-) embryos

124 Here we show that E2f4-deficiency leads to an absence of ciliated cells fr

125 The E2F4-deficient progenitor cells showed reduced expressio

126 type p53-mediated inhibition of UBE2C is p21-E2F4-dependent and GOF mutant p53-mediated transactivati

127 y the cyclin kinase inhibitor p16(INK4a), an E2F4-dependent process.

128 4A) pulse, abolishing the shift from E2F3 to E2F4, derepressing E2F target genes, and expanding a ste

129 nizing centres and that, without cytoplasmic E2f4, deuterosomes are not assembled, halting multicilio

130 Trim28 depletion increased E2F3 and E2F4 DNA binding activity, as measured by chromatin-immu

131 006474 resulted in the loss of intracellular E2F4 DNA-binding activity as measured by electrophoretic

132 Unlike E2F1, E2F4 does not induce apoptosis, and this correlates with

133 vator E2F1 to complexes containing repressor E2F4, downregulating BRCA1 expression.

134 DREAM contains p130, E2F4, DP1, and a stable core complex of five MuvB-like p

135 core interacts with Rb-like protein p130 and E2F4-DP1 to form the DREAM complex that mediates global

136 enetically repressing XPC and inhibiting the E2F4/DP1 complex.

137 the known crystal structure of the DNA-bound E2F4/DP2 heterodimer.

138 n of genes repressed by quiescence-promoting E2F4/DREAM complex.

139 hat the ability of HDAC1 to repress E2F3 and E2F4-driven transcription is dependent on Trim28.

140 es, two other kinases, transcription factors E2F4, E2F5, and p130, a DNA repair gene, a gene for the

141 E2F1, E2F2, and E2F3a) or repressors (E2F3b, E2F4, E2F5, E2F6, and E2F7).

142 Downstream E2F4/E2F5 targets, which are potentially involved in the

143 l of cell cycle transcription factors (E2F1, E2F4, E2F6, and GABPA) from the Encyclopedia of DNA Elem

144 These Rb(-/-);E2f4(-/-) embryos exhibited all of the defects character

145 d a conditional mouse model to allow Rb(-/-);E2f4(-/-) embryos to develop in the presence of Rb wild-

146 E2F4 export is mediated by two hydrophobic export sequen

147 hese data suggest that changes in necdin and E2F4 expression after rosiglitazone exposure in humans a

148 E2F4 expression was decreased by 10-fold in muscle and 2

149 RBL2/E2F4 formation in turn led to a shift in BRCA1 promoter

150 scriptional program of centriole biogenesis, E2f4 forms apical cytoplasmic organizing centres for ass

151 lear export contributes to the regulation of E2F4 function, including its ability to regulate exit fr

152 Furthermore, E2F4 functionally interacts with chromatin regulators as

153 nally differentiated cells, common KDM5A and E2F4 gene targets were bound by the pRB-related protein

154 nesis, transgenic mouse lines expressing the E2F4 gene under the control of a keratin 5 (K5) promoter

155 o the 3'-untranslated region (3'-UTR) of the E2F4 gene.

156 t inducer of apoptosis whereas its relative, E2F4, generally does not promote cell death.

157 As Rb(-/-);E2f4(-/-) germline mice die in utero, we generated Rb(-/

158 We found that loss of E2f4 had a differential effect on known Rb-associated ne

159 Remarkably, loss of E2F4 had no detectable effect on either cell cycle arres

160 cription start site regions independently of E2F4; however, it cooperated with E2F4 to promote a stat

161 These findings emphasize the significance of E2F4 in controlling gene expression and cell fate.

162 ed by interplay between Sp1, p107, p130, and E2F4 in distinct transcriptional complexes during skelet

163 ell cycle genes and E2F targets upon loss of E2F4 in RB family-mutant cells.

164 on heterologous promoters and binds to p130/E2F4 in response to overexpression of p53.

165 he -401 TIE was capable of binding Samd3 and E2F4 in TGFbeta-treated cells.

166 ket protein is required to act downstream of E2F4 in the differentiation process.

167 We investigated the role of E2F4 in the genotoxic stress response.

168 To examine the role of E2F4 in tumor development, the mouse skin two-stage carc

169 RB family/E2F complexes, which includes p130/E2F4, in response to genotoxic agents, is not well under

170 on of VSMCs leading to increased IH, whereas E2F4 inhibits this pathological response.

171 Thus, E2f4 integrates nuclear and previously unsuspected cytop

172 ether, these findings show that p130 escorts E2F4 into the nucleus and, together with corepressor com

173 E2F4 is a transcriptional repressor implicated in cell c

174 We have found that E2F4 is actively exported from the nucleus and that lept

175 E2F4 is an E2F family member that has been proposed to b

176 Here, we demonstrate that E2F4 is highly upregulated following the neuronal differ

177 Here we show that E2F4 is important for the proliferation and the survival

178 This suggests that E2F4 is important in early stages of commitment to the l

179 This role for E2F4 is independent of the RB family.

180 The separation of Mip/LIN-9 from p107,p130/E2F4 is likely driven by phosphorylation of the pocket p

181 ree E2F DNA binding activity is reduced, and E2F4 is primarily nuclear.

182 We therefore conclude that E2f4 is required to determine the appropriate developmen

183 E2F4 is the major pRB-associated E2F in vivo, yet its ro

184 E2F4 is the most abundant E2F protein in many cell types

185 In contrast, E2F4 is unable to bind to the -143/+10 region of the Mcl

186 We propose that E2F4 is unable to repress the Mcl-1 promoter primarily a

187 rom the binding site by AR and replaced with E2F4, leading to the recruitment of the silencing mediat

188 The IR-induced increase of E2F4 levels led to an increase in E2F4 binding to p130 b

189 In addition, in the proximal lung, E2f4 loss causes a reduction in Clara cell marker expres

190 t striking effect was in the pituitary where E2F4 loss delayed the development, and reduced the incid

191 In addition, E2F4 loss does not override the differentiation defect r

192 This suggests that E2F4 makes a major contribution to the control of erythr

193 showed histone modifications suggesting that E2F4 may function as a long-range regulator, which we co

194 E2f4-/- mice died of an increased susceptibility to oppo

195 icularly striking in the nasal epithelium of E2f4-/- mice where ciliated cells are replaced by column

196 ografts and primary HGSOC tumors, ZC3H18 and E2F4 mRNA levels are positively correlated with BRCA1 mR

197 lite repeats in the TGFbetaIIR, IGFIIR, BAX, E2F4, MSH3, MSH6, BRCA1, and BRCA2 genes were generally

198 tions that causes the postnatal lethality of E2f4 mutant mice.

199 f trophectoderm-like cells in both Rb and Rb;E2f4 mutant placentas.

200 Using genetically altered mice and E2F4 mutant proteins we demonstrate that centriole ampli

201 Under these conditions, Rb(-/-);E2f4(-/-) mutants survived to birth.

202 ic binding to DNA of the c-Fos, c-Jun, E2F1, E2F4, MyoD, myogenin, and c-Myc transcription factors.

203 factors including c-Fos, c-Jun, AP-2, E2F1, E2F4, NF-kappaB, MyoD, and myogenin.

204 l set of motifs, including GABPA, MYC, E2F1, E2F4, NRF-1, CCAAT, YY1, and ACTACAnnTCC are overreprese

205 p130 deficiency triggered a dramatic loss of E2F4 nuclear localization as well as transcriptional der

206 E2F4-null mouse embryonic fibroblasts were less sensitiv

207 E2F4 occupies promoter regions of proapoptotic factors,

208 E2F4 often represents the predominant E2F activity in ce

209 monstrate that while the effects of E2F1 and E2F4 on cell proliferation in vivo are similar, their ap

210 d p130 formed transcriptional complexes with E2F4 on the FGFR1 promoter and repressed FGFR1 gene tran

211 mediated through switching between E2F1 and E2F4 on the promoter of cyclin B1.

212 al recruitment of E2F3 by EWS-FLI1 replacing E2F4 on their target promoters.

213 does not affect its ability to interact with E2F4 or cyclins.

214 cilin acts by forming a ternary complex with E2f4 or E2f5 and Dp1 that binds and activates most of th

215 Interaction between NS1 and E2F4 or E2F5 enhanced the nuclear import of these repres

216 adipocytes with rosiglitazone did not alter E2F4 or necdin, expression of both genes was significant

217 ath while interference with the synthesis of E2F4 or p130, or with the interaction of E2F4-p130 with

218 posttranscriptional increase in the level of E2F4, p105(Rb), and p130 and induced the formation of nu

219 g the replacement of free E2F complexes with E2F4-p105(Rb) complexes.

220 duced the formation of nuclear E2F4-p130 and E2F4-p105(Rb) complexes.

221 directly regulated by unique combinations of E2F4, p107, and p130, including a group of genes specifi

222 emonstrated that Sp1 interacted with p107 in E2F4-p107 transcriptional complexes in myoblasts.

223 ed muscle fibers by the relative loss of the E2F4-p107-Sp1 transcription complex and replacement by t

224 in E2F4 binding to p130 but had no effect on E2F4/p107 or E2F5/p130 complexes.

225 The E2F4/p107/cyclin E/CDK2 complex, a minor component in pr

226 nd p130 and induced the formation of nuclear E2F4-p130 and E2F4-p105(Rb) complexes.

227 E2F4-p130 becomes the predominant E2F-pocket complex for

228 ion complex and replacement by the repressor E2F4-p130 complex.

229 Following stress exposure, E2F4-p130 complexes are lost rapidly along with the pres

230 vity, dissociation of cyclin A-CDK2 from the E2F4-p130 complexes, and inhibition of G(1)/S transition

231 of E2F2 and E2F4, and the growth-suppressive E2F4-p130 complexes.

232 of E2F4 or p130, or with the interaction of E2F4-p130 with chromatin modifiers, induces neuron death

233 and death are dependent on the integrity of E2F4-p130-HDAC/Suv39H1 complexes.

234 Following mitogenic stimulation, repressive E2F4-p130-histone deacetylase complexes dissociate from,

235 The increase in E2F4/p130 association after IR was observed in prostate

236 E2F4/p130 complex formation was dependent on dissociatio

237 ar accumulation, leading to the formation of E2F4/p130 complexes and increased occupancy of E2F4 and

238 3/pRB by constitutively expressed repressive E2F4/p130 complexes on target genes upon EWS-FLI1 modula

239 poxia is specifically mediated by repressive E2F4/p130 complexes that bind to a single E2F site in th

240 gram mediated by the formation of repressive E2F4/p130 complexes that represents an integral response

241 the BRCA1 and RAD51 promoters by repressive E2F4/p130 complexes, a pathway prevented by expression o

242 n, as was the cdk4-dependent dissociation of E2F4/p130 complexes.

243 at the transcriptional level via repressive E2F4/p130 complexes.

244 The E2F4/p130 pocket protein complex emerges as a new target

245 Thus, Rb and E2f4 play cooperative roles in placental development.

246 to E2F1 and E2F3, which sensitize to death, E2F4 plays a crucial protective role in neuronal death e

247 Taken together, we propose a model by which E2F4 plays a protective role in neurons from ischemic in

248 mplex, whose key components include p130 and E2F4, plays a fundamental role in repression of cell cyc

249 Finally, our results indicate that E2F4 promoter occupancy is globally associated with p53-

250 M006474 resulted in down-regulation of total E2F4 protein as well as known E2F targets.

251 The E2F4 protein is involved in gene repression and cell cyc

252 E2F4 protein levels increased and accumulated in the nuc

253 the E2F4 antisense transcript and decreased E2F4 protein levels.

254 The antisense-mediated decrease in E2F4 protein was reflected by reduced E2F4 association w

255 essor pathway and the assembly of repressing E2F4-Rb DNA binding complexes.

256 p130 "form 3," which does not interact with E2F4, readily interacts with E2F1.

257 Moreover, abrogation of E2F4 recruitment via the inactivation of RB pocket prote

258 Rb and the subsequent association of the Rb/E2F4 repressive complex to CDE/CHR elements in the proxi

259 o E2F promoters where it eliminates p130 and E2F4, resulting in the dramatic elimination of H3 Lys-9

260 Analysis of newborn pups deficient in E2F4 revealed abnormalities in hematopoietic lineage dev

261 t other E2Fs, and it occurs independently of E2F4's ability to interact with pocket proteins.

262 terference RNA (siRNA)-mediated knockdown of E2F4 sensitized cells to subsequent irradiation, resulti

263 and increased phosphorylation and decreased E2F4 sequestering ability of the CDK4 target, p130/Rb2.

264 of the defects characteristic of the Rb and E2f4 single mutants and had no novel defects.

265 resses Brca1 transcription by binding to the E2F4 site of the Brca1 promoter.

266 0 hyperphosphorylation, dissociation of p130-E2F4-Suv39H1-HDAC complexes, altered modification of H3

267 rt of a Sin3 complex and that on a subset of E2F4 target genes, the coordinated activity of Sin3 and

268 d to permanent gene silencing on a subset of E2F4 target genes.

269 Downstream E2F4 targets potentially involved in the progression fro

270 ur findings uncover a non-canonical role for E2F4 that provide insights into the biology of rapidly d

271 inding targets of human transcription factor E2F4 that we independently validated by promoter-specifi

272 E2F4, the most abundant E2F protein, is thought to act i

273 Disruption of E2F4 through small interfering RNA prevented p130/E2F4 c

274 1) with the p130 or p107 pocket proteins and E2F4 to a transcriptionally active complex in S-G(2) con

275 promoter where it facilitates recruitment of E2F4 to an adjacent E2F site to promote BRCA1 transcript

276 oblastoma protein p130/Rb2, which sequesters E2F4 to block entry into G1, 10-fold elevated levels of

277 to E2F3a) and upregulating repressive E2Fs (E2F4 to E2F8) in the primary CD36(+) EPCs.

278 The ability of E2F4 to prevent adipogenesis seems to be quite distinct

279 ndently of E2F4; however, it cooperated with E2F4 to promote a state of deepened repression at cell c

280 onally, we detected binding of both E2F1 and E2F4 to the Rb promoter in vivo using chromatin immunopr

281 lls, free E2F DNA binding activity (E2F2 and E2F4, to a lesser extent E2F1, E2F3, and occasionally E2

282 lation of residues S650 and S975 weakens the E2F4 transactivation domain binding.

283 nct residues regulates p107 affinity for the E2F4 transactivation domain.

284 ian cells in culture, to dissociate the p130-E2F4 transcription factor complex, and to stimulate ATP

285 that the promoters of 127 were bound by the E2F4 transcription factor in primary fibroblasts.

286 substantial portion of target genes with the E2F4 transcription factor.

287 Furthermore, expression of E2F1, but not E2F4, transcription factor in mouse fibroblasts represse

288 Unlike E2F1 transgenic mice, E2F4 transgenic mice developed skin tumors with a decrea

289 E2F4 was always nuclear in limbal epithelium and cytopla

290 However, E2F4 was essential for normal development.

291 een observed in vitro, ectopically expressed E2F4 was found to localize to the nucleus and induce pro

292 omoter activity, repression by E2F1, but not E2F4, was enhanced by the coexpression of pRB.

293 atin immunoprecipitated using an antibody to E2F4, we have identified 68 unique target loci; 15% are

294 owed that expression of cyclin D1, CDK2, and E2F4 were increased, and Rb levels were decreased in the

295 Some genes (e.g., E2F4) were overexpressed in tumor epithelial cells and s

296 ted the transcriptional activity of E2F3 and E2F4, whereas Trim28 deficiency enhanced their activity.

297 This contrasts with the effects of E2F4, which enhances the differentiation state of PC12 c

298 bpalpha, which enforces differentiation, and E2F4, which suppresses cell-cycle re-entry.

299 activity, enhancing the binding of p130 and E2F4, which together bind to and repress the cdc2 promot

300 oscopy indicated co-localization of E2F3 and E2F4 with Trim28 within the cell nucleus, and co-immunop