ライフサイエンスコーパス: E2F1

1 E2F1 and retinoblastoma (RB) tumor-suppressor protein no

2 E2F1 binds less cyclin A but more target promoters when

3 E2F1 is a fibrogenic gene and could serve as a potential

4 E2F1 is acetylated in response to DNA damage but the rol

5 E2F1 is tightly controlled by multiple mechanisms, but w

6 E2F1 is well known to promote G1 cell cycle progression,

7 E2F1 loss accelerated tumor growth, while E2F2 and E2F3

8 E2F1 regulates ABCG2 expression in multiple cell systems

9 E2F1 specifically has been shown to be a critical mediat

10 E2F1 targets included glycolysis and metabolic genes inc

11 E2F1 was also highly induced by 3,5-diethoxycarbonyl-1,

12 E2F1, E2F2, and E2F3A interact with the cyclin box of cy

13 E2F1, E2F2, and E2F3A, the three activators of the E2F f

14 E2F1, MEF2C, and TOX proteins were decreased with miR-22

15 E2F1-/- mice exhibited reduced biliary fibrosis by DDC a

16 xpression of the E2F transcription factor 1 (E2F1) and loss of retinoblastoma 1 (RB1).

17 E2F transcription factor 1 (E2F1) is an important regulator of metabolic diseases; h

18 e findings delineate a pRb-Skp2-p27-cyclin A-E2F1 pathway that determines whether E2F1 is proliferati

19 In addition, it activates E2F1-target genes in a methyltransferase activity-indepe

20 g SIRT1 activity and consequently activating E2F1-dependent ARF transcription.

21 , these E2F members, in particular activator E2F1 and repressors E2F7 and E2F8, form a feedback circu

22 p53 and homologs p63/p73, but did not affect E2F1, TCF1, and c-Myc.

23 es not deubiquitinate UbK48 chains or affect E2F1 protein stability.

24 Different viruses affect E2F1/retinoblastoma (Rb) interactions by diverse mechani

25 3 physically interacts with PARP-1 affecting E2F1 transcriptional activity.

26 Although E2F1 and DP1 increased without Rb suppression, the E2F1

27 p27T187A KI activated an E2F1-p73-apoptosis axis in DKO prostate tumorigenesis, s

28 dentify SENP3, a desumoylating enzyme, as an E2F1-interacting partner.

29 cy and transcriptome profiling identified an E2F1- and E2F3B-driven transcriptional program that was

30 sses Cyclin E gene (CCNE1) transcription, an E2F1 activated gene that is also repressed by the Retino

31 e was significantly more beta-arrestin-1 and E2F1 associated with these promoters in human NSCLC tumo

32 enhanced recruitment of beta-arrestin-1 and E2F1 on vimentin, fibronectin, and ZEB1 and ZEB2 promote

33 transcription factors (SREBP-1, SREBP-2, and E2F1) in liver.

34 associated with low p14-ARF increase AR and E2F1 transcriptional activity and promote the developmen

35 2A.Z.2-regulated genes are bound by BRD2 and E2F1 in an H2A.Z.2-dependent manner.

36 ogenic transcripts such as HIF1A, CCND1, and E2F1.

37 ression independently of RB1 degradation and E2F1 activation.

38 contribution of dysregulated C/EBPalpha and E2F1 to elevated Trib2 expression and leukemic cell surv

39 is enriched for cell cycle related genes and E2F1 targeted genes, plays a role in the molecular diffe

40 stantial overlap with H3K9me3, H3K27me3, and E2F1 transcriptional factor binding.

41 osure alone led to H3K9 hyperacetylation and E2F1 binding at the FOS promoter, which remained elevate

42 RANKL-induced expression of inflammatory and E2F1 target genes and downstream osteoclastogenesis.

43 nally, reduction of p-RB(Ser-780) levels and E2F1 target gene expression upon ectopic expression of R

44 tion factor binding sites for p53, MEF2A and E2F1 were significantly (P < 0.05) over-represented in S

45 reviously unknown mechanism in which RBF and E2F1 modify Hippo signaling responses to modulate apopto

46 lts reveal a novel link between RORalpha and E2F1 in regulating cell cycle progression and mammary ti

47 family, heat-shock factor 1, ATF6, SRF, and E2F1 transcription factors.

48 We demonstrate that E2F1 mRNA stability and E2F1 protein levels are reduced in cells lacking RALY ex

49 g a positive feedback loop between UCH37 and E2F1.

50 a transcriptional repressor that antagonizes E2F1 at the crossroads of the cell cycle, apoptosis, and

51 sion of both proliferative and pro-apoptotic E2F1 target genes.

52 as Wnt signaling and promoter motifs such as E2F1 and TCF3.

53 modulating DNA methylation (i.e., Uhrf1), as E2F1 targets.

54 F occupancy and histone acetylation marks at E2F1-target promoters.

55 s triggered a positive feedback loop via ATM/E2F1/STAT signaling, amplifying the TRIM37 network in ch

56 tive stress inhibits the interaction between E2F1 and SENP3, which leads to accumulation of sumoylate

57 E2F1 (S29A) prevents the interaction between E2F1 and TopBP1 and recruitment of RB, E2F1, and BRG1 to

58 In humans, Rb binds E2F1-E2F5, whereas p107 and p130 almost exclusively asso

59 factor E2F7 competed against DP1 and blocked E2F1-induced KPNA2 gene activation.

60 A knock-in mutation that blocks E2F1 acetylation abolishes the recruitment of p300 and C

61 Egr-1 promoter was activated by E2F1, and the activation was abrogated by expression of

62 nterestingly, UCH37 expression is induced by E2F1, and its level rises in G1/S transition and S phase

63 illustrate a dynamic regulation of Rad51 by E2F1 and p53 in prostate cancer cells' response to hypox

64 Upregulation of Rad51 by E2F1 upon DNA damage under hypoxia contributed to such r

65 anscription factor, FOXM1 is is regulated by E2F1 which also controls TYMS.

66 les during development and are suppressed by E2F1.

67 yclin B2, cyclin D1, cyclin E2, cdc6, cdc20, E2F1, and MCM complexes in DHX33 knockout embryos.

68 We find that SCF-cyclin F controls E2F1 ubiquitylation and degradation during the G2/M phas

69 Conversely, E2F1-deficient mouse fibroblasts had increased Ogt and M

70 Skp2 deletion or p27T187A mutation converts E2F1's role from proliferative to apoptotic.

71 involved in the cell cycle, notably cyclin, E2F1, cell division cycle (CDC), and minichromosome main

72 cell-cycle-related gene (cyclins A1, A2, D1, E2F1, and PCNA) and protein (cyclin D1 and CDK4) express

73 tionally regulated and involve DDR-dependent E2F1 transcription factor activity.

74 pecific downregulation of the FOXO-dependent E2F1 transcriptional program in multiple cancer types an

75 ut partially resulted from the downregulated E2F1.

76 onstrate that interaction between Drosophila E2F1 and Sd disrupts Yki/Sd complex formation and thereb

77 ch was caused by deregulation of cyclin D/E, E2F1, RB1, and increased Myc activity.

78 ntranslated regions (UTRs) of E2F1 and E2F3 (E2F1/3) mRNAs.

79 profiles of several cellular factors (E2F6, E2F1, Rb, HDAC1, and HDAC2) together with EBV latent nuc

80 P2A, AURKA, CKS2, CCNB2, CDK1 SLC19A1, E2F8, E2F1, PRC1, KIF11 for in depth validation.

81 d a significant correlation between elevated E2F1 and ABCG2 expression in human lung cancers.

82 ds to the ribosomal protein RPL35 to enhance E2F1 protein synthesis, leading to DEPDC1B gene transcri

83 romoter-specific hyperacetylation facilitate E2F1-mediated FOS induction in As2O3-induced cellular tr

84 and downstream targets transcription factor E2F1 and cycling-dependent kinase 2 (CDK2), thereby reve

85 A typical transcription factor E2F1 associated with its DNA-binding partner DP1 bond to

86 the nucleus, leading to transcription factor E2F1 hyperactivation.

87 on accumulation of the transcription factor E2F1 in cyclin F-depleted cells.

88 Moreover, the transcription factor E2F1 induces EZH2 during the GC reaction.

89 calized TyrRS activates transcription factor E2F1 to upregulate the expression of DNA damage repair g

90 (AMPK) and the nuclear transcription factor E2F1, detailed auditory pathology was not delineated.

91 Deregulation of the transcription factor E2F1, normally repressed by CCAAT enhancer-binding prote

92 ically activated by the transcription factor E2F1--a factor perturbed in the majority of human cancer

93 -kappaB signaling and a transcription factor E2F1-dependent metabolic pathway by the cytokine RANKL.

94 inked to suppression of transcription factor E2F1-mediated cell cycle regulation.

95 x 1-S6K pathway and the transcription factor E2F1.

96 acetylase SIRT1 and the transcription factor E2F1.

97 und by the S-phase gene transcription factor E2F1.

98 0.9006 for ZFX, 0.8892 for ESRRB, 0.8920 for E2F1.

99 in Rb results in an increase in affinity for E2F1 and E2F2 and an increase in the ability of p107 to

100 clins, including D-type cyclins critical for E2F1 activation, were dependent on K19 expression, and K

101 o our knowledge, deubiquitinating enzyme for E2F1.

102 and identify a feedback regulatory loop for E2F1, C/EBPalpha, and Trib2 in AML cell proliferation an

103 These results uncover a novel mechanism for E2F1 transcriptional activation through removal of its L

104 Of the known binding partners for E2F1, we queried whether retinoblastoma 1 (Rb1) might be

105 mRNA translation stress-response pathway for E2F1 activation that is exploited by EBV to promote cell

106 ression, suggesting that Rb1 is required for E2F1-mediated suppression.

107 These findings reveal an important role for E2F1 acetylation in orchestrating the remodeling of chro

108 f E2F1 knockout tumors identified a role for E2F1 as a master regulator of a suite of pro-metastatic

109 Here we demonstrate a pivotal role for E2F1, a cell cycle regulatory transcription factor, in c

110 edures included cell cycle associated genes (E2F1, CCND1, FOXM1, TP53, and RB1), transcription factor

111 ral E2F1 protein expression was either high (E2F1(high)) or low (E2F1(low)).

112 egulation of Fgf13 may partially explain how E2F1 promotes breast cancer metastasis.

113 However, E2F1 promotes both proliferation and apoptosis.

114 Further, we found that human E2F1 competes with YAP for TEAD1 binding, affecting YAP

115 Here, we identified E2F1 and E2F3 mRNAs as translational targets of WDR77.

116 Together, these data identify E2F1 as a key transcription factor modulating the expres

117 Collectively, our results identify E2F1/FOXO cooperation as a regulatory mechanism that pla

118 rylates and how this phosphorylation impacts E2F1 activity in general is not known.

119 The S29A mutation impairs E2F1 stabilization in response to ultraviolet (UV) radia

120 SF15), and their receptors, were enriched in E2F1(high) While TRAIL was equally expressed in adipocyt

121 ed subtle but impactful copy number gains in E2F1 and E2F3 in hepatocellular carcinoma (HCC).

122 d inhibited the MAGE-A11-induced increase in E2F1 transcriptional activity.

123 The amino-acid residue in E2F1 that CDK8 phosphorylates and how this phosphorylati

124 3 targets with oncogenic function, including E2F1 and MEF2C, and the predicted miR-223 target, TOX, r

125 tivity of additional oncoproteins, including E2F1 and AKT.

126 1 suppressed cell-cycle regulators including E2F1, E2F2, EXO1, FOXM1, and MCM2.

127 p14-ARF and cooperated with HDM2 to increase E2F1 transcriptional activity in the absence of p14-ARF.

128 causes Rb degradation and uses the increased E2F1 and DP1 factors to transcribe viral genes.

129 Binding of RORalpha inhibited E2F1 acetylation and its DNA-binding activity by recruit

130 revents cyclin A from binding and inhibiting E2F1.

131 n and degradation of DP1, thereby inhibiting E2F1-DP1 activity.

132 Oxidative stress inhibits E2F1 transcriptional activity, independent of changes in

133 Interestingly, E2F1 activated Egr-1 expression in a biphasic fashion as

134 udy unraveled a regulatory cascade involving E2F1, early growth response-1 (Egr-1), nuclear receptor

135 n of a new pathway mediated by uL3 involving E2F1 and Cyclin D1 in the regulation of cell cycle progr

136 These studies suggest that this KRAS-E2F1-ILK-hnRNPA1 regulatory loop enables pancreatic canc

137 Cells lacking E2F1 are hypersensitive to oxidative stress due to the d

138 Liver E2F1 messenger RNA (mRNA) and protein expression was str

139 ression was either high (E2F1(high)) or low (E2F1(low)).

140 and thereby represses expression of the LSD1-E2F1 cotarget genes, but has no effects on H3K4me2 level

141 PHF8 decreases the H3K4me2 level at the LSD1-E2F1 cotargeted loci, but this effect is rescued by code

142 In murine models, E2F1 expression and activity increased in response to fe

143 ne 266 residue, which specifically modulates E2F1 transcriptional activity to enhance cell cycle arre

144 Moreover, E2F1 expression was increased in liver biopsies from obe

145 TP53, and RB1), transcription factors (Myc, E2F1, TBX2, FOXM1), DNA replication regulators (CDKN1A,

146 iving NEPC including Aurora Kinase A, N-Myc, E2F1 and STAT3.

147 lusive whether the hyper-phosphorylated, non-E2F1-interacting form of Rb has any physiological role.

148 Accumulation of endogenous p53 but not E2F1 and suppressed RAD51 transcription was observed in

149 report a lineage-specific decline of nuclear E2F1 during differentiation of rodent OPC into oligodend

150 ock-in mouse model thus links the ability of E2F1 to directly promote DNA repair with the suppression

151 In the absence of E2F1 and E2F2, however, repression of E2F3 elicits profo

152 -223 expression, likely due to activation of E2F1, a known repressor of miR-223 transcription.

153 Activation of E2F1, on overexpression of its activator CCND1 (cyclin D

154 d p53 binding, resulting in re-activation of E2F1-dependent apoptosis and blockade of mutp53 gain-of-

155 er, our data suggest oncogenic activities of E2F1 and E2F3 in ErbB2- or Myc-triggered mammary tumorig

156 ly regulated the transcriptional activity of E2F1 on DNA replication genes.

157 ly regulates the transcriptional activity of E2F1 on DNA replication genes.

158 hat uL3 negatively regulates the activity of E2F1 promoter.

159 lly rescued transcription factor activity of E2F1 that was repressed by RORalpha.

160 assays further confirmed the association of E2F1, SHP, and EID1 proteins with the Egr-1 promoter, an

161 Binding of E2F1 to chromatin on the gene targets was validated and

162 ased methodology, exemplified in the case of E2F1-induced aggressive tumors, has the potential to sup

163 nthesis of DNA, mostly through disruption of E2F1 and its target genes.

164 Rb/E2F1 complex, leading to dissociation of E2F1 and enhanced OPC proliferation.

165 on residues of E2F7 or DNA-binding domain of E2F1 abolished the suppressive effects of E2F7 on KPNA2

166 RCA1 promoter and blocking the enrichment of E2F1 on BRCA1 promoter.

167 with AKT inhibitors suppresses expression of E2F1 and p73 without interfering with ATR signaling.

168 Increased expression of E2F1 gene targets was also detected in mouse gliomas (th

169 Elevated expression of E2F1 in adipocyte fraction of human visceral adipose tis

170 Moreover, the expression of E2F1 proliferative and pro-apoptotic genes is correlated

171 and inversely correlated with expression of E2F1 target genes and cell proliferation.

172 at Rb1 deletion induces higher expression of E2F1 target genes in the absence of Skp2.

173 opBP1 positively regulates the expression of E2F1, a TopBP1-binding partner, and p73 in HPV-positive

174 3 in MF/CTCL lead to increased expression of E2F1, MEF2C, and TOX, which likely contributes to the de

175 ance and highlight a radical new function of E2F1 that is relevant to tumor therapy.

176 le progression and levels of target genes of E2F1, a key transcriptional factor for the transition in

177 -deficient cells exhibit hypersumoylation of E2F1 and are resistant to oxidative insult.

178 f E2F7/8 triggers apoptosis via induction of E2F1 in response to stress, indicating that the tumor-pr

179 results in PI3Kdelta-dependent induction of E2F1 mRNA translation with the consequent activation of

180 Levels of E2F1 and both mRNA and protein of SKP2 were increased in

181 tion, KPNA2 mediated nuclear localization of E2F1 and E2F7, where they in turn controlled KPNA2 expre

182 e G1 cell cycle progression, and the loss of E2F1 in SmgGDS-depleted cells provides an explanation fo

183 Strikingly, it was observed that loss of E2F1 or E2F2 significantly reduced the metastatic capaci

184 and Mgea5 expression, yet overexpression of E2F1 in the Rb1-deficient cells did not alter Ogt and Mg

185 Phosphorylation of E2F1 also leads to the recruitment of E2F1 to sites of D

186 nalysis demonstrates that a large portion of E2F1 and LSD1 cotargeted genes are involved in cell cycl

187 In contrast, the presence of E2F1 at B-Myb sites increases with stress.

188 Transcriptomic profiling of E2F1 knockout tumors identified a role for E2F1 as a mas

189 UCH37 localizes to the promoters of E2F1 pro-apoptotic target genes such as caspase 3, caspa

190 pies could be of utility in the promotion of E2F1-dependent apoptosis in cancer cells, in avoiding me

191 ion of E2F1 also leads to the recruitment of E2F1 to sites of DNA damage, where it functions to enhan

192 o the heptad repeat and marked box region of E2F1 and suppressed E2F1-regulated transcription in epit

193 CR analyses demonstrate the up-regulation of E2F1 target apoptotic genes (Bnip3 and p53inp1) in Kbtbd

194 B(Ser-780)) followed by the up-regulation of E2F1 target genes required to promote G1 to S phase tran

195 muscle myogenesis through the regulation of E2F1-DP1 activity.

196 cer cell proliferation through regulation of E2F1-driven DNA metabolism and replication genes togethe

197 ctly involved in translational regulation of E2F1/3 mRNAs through their structured 5' UTRs, PDCD4, an

198 omitant phosphorylation of Rb and release of E2F1.The histone methyltransferase EZH2 silences genes b

199 erplay between KRAS and ILK and the roles of E2F1, c-Myc and heterogeneous nuclear ribonucleoprotein

200 ated that WDR77 regulated the translation of E2F1 and E2F3 mRNAs through the 5' untranslated regions

201 ecreases the Lys-63-linked ubiquitination of E2F1 and activates its transcriptional activity.

202 hrough the 5' untranslated regions (UTRs) of E2F1 and E2F3 (E2F1/3) mRNAs.

203 DNA double-strand breaks (DSBs) dependent on E2F1 and ATM kinase activity and promotes DSB repair thr

204 t of its E3 ligase activity but depending on E2F1, a well-known transcription factor of BRCA1 promote

205 romoting transcription factor, we focused on E2F1.

206 mutation of the ATM phosphorylation site on E2F1 (S29A) prevents the interaction between E2F1 and To

207 In HEK293 cells, we overexpressed E2F1, which significantly reduced OGT and MGEA5 expressi

208 ration as a regulatory mechanism that places E2F1 apoptotic activity under the control of survival si

209 escence programs dampening the cyclin D1-pRb-E2F1 pathway.

210 creasing the abundance of the inhibitory pRB-E2F1 complex and limiting G0/G1 arrest.

211 ssor protein/E2 promoter binding factor (pRb/E2F1) pathway, which we have previously established as a

212 further determined that TGFbeta induces pRb/E2F1-dependent transcriptional activation of several aut

213 at TGFbeta induces autophagy through the pRb/E2F1 pathway and transcriptional activation of autophagy

214 r highlight the central relevance of the pRb/E2F1 pathway downstream of TGFbeta signaling in tumor su

215 As expected, the S29A mutation prevents E2F1 association with damaged DNA and reduces DNA repair

216 Suppression of PI3Kdelta prevents E2F1 activation also in non-EBV-infected cells.

217 e) by the ATM or ATR kinases, which promotes E2F1 protein stabilization.

218 g protein RPL35 as key factors for promoting E2F1 protein synthesis, N-Myc protein stability and N-My

219 The transcription factors RB, E2F1 and E2F7 bind to a subset of DREAM target genes tha

220 tween E2F1 and TopBP1 and recruitment of RB, E2F1, and BRG1 to DSBs.

221 C/EBPbeta-LIP also disrupts Rb-E2F1 complexes in C/EBPalpha-S193D mice after CCl4 treat

222 hk1's expression is controlled by p53 and RB/E2F1 at the transcriptional level.

223 ase onset in conjunction with increase in Rb/E2F1-mediated cyclin E1 expression, but reduced levels o

224 1 deacetylates retinoblastoma (Rb) in the Rb/E2F1 complex, leading to dissociation of E2F1 and enhanc

225 IF1A, STAT4, ATF4, TP63, EGR1, CDKN2A, RBL1, E2F1, PRDM1, GATA3, and IRF4) at 18 hours after exposure

226 er types and by the association of a reduced E2F1/FOXO transcriptional program with poor prognosis.

227 RBF modifies these effects by reducing E2F1/Sd interaction.

228 The cell cycle regulators E2F1, MYC, MYBL2 (B-Myb) and FOXM1 are among the DREAM t

229 interactions by diverse mechanisms releasing E2F1 from its suppressor Rb, enabling viral replication.

230 rates with SUV39H1 and RB protein to repress E2F1-dependent CCNE1 transcription.

231 t therefore remains unclear how de-repressed E2F1 promotes tumorigenesis.

232 cancer, TopBP1 forms oligomers and represses E2F1-dependent apoptosis.

233 m of tumour suppression by pRb is repressing E2F1.

234 ility of RB loss to differentially reprogram E2F1 in human cancers.

235 their ability to repress the E2F-responsive E2F1 promoter.

236 ors, which eventually results in restraining E2F1 activity, restored miR-223 expression and miR-223 a

237 Thus, Cyclin F restricts E2F1 activity during the cell cycle and upon checkpoint

238 ENP3 across numerous cancer types, the SENP3-E2F1 axis may serve as an avenue for therapeutic interve

239 phagy and MAP3K5 (ASK)-MAP kinase signaling, E2F1 governs a distinct transcriptome that contributes t

240 Specifically, E2F1 negatively regulates both Ogt and Mgea5 expression

241 3, which leads to accumulation of sumoylated E2F1.

242 and marked box region of E2F1 and suppressed E2F1-regulated transcription in epithelial cells.

243 ta inhibitor Idelalisib (CAL-101) suppresses E2F1 and c-Myc levels and causes cell death in EBNA1-ind

244 ted HDAC1 from deacetylating and suppressing E2F1.

245 ct on BRCA1 expression and HR by suppressing E2F1-mediated transactivation of BRCA1 promoter and bloc

246 stimulates the expression of FBP in a TFDP1/E2F1-dependent manner.

247 Here we demonstrate that E2F1 acetylation creates a binding motif for the bromodo

248 We demonstrate that E2F1 deficiency leads to a decrease in glycolysis and de

249 We further demonstrate that E2F1 directly binds to the promoters of key lipogenic ge

250 We demonstrate that E2F1 mRNA stability and E2F1 protein levels are reduced

251 In conclusion, our data demonstrate that E2F1 regulates lipid synthesis and glycolysis and thus c

252 in both human and mouse cells and found that E2F1 bound to candidate E2F binding sites in both promot

253 eover, by using siRNA to E2F1, we found that E2F1 was essential for the activity of the U79 promoter.

254 Here, we reveal that E2F1 plays an essential role in liver physiopathology th

255 Further analyses revealed that E2F1-mediated Trib2 expression was repressed by C/EBPalp

256 We show that E2F1 causes chemotherapeutic drug efflux both in vitro a

257 We further show that E2F1 is important for E6 to upregulate Cdk1.

258 The E2F1/FOXO axis is frequently blocked in cancer, as evide

259 cted with human herpesvirus 6A (HHV-6A), the E2F1 protein and its cofactor DP1 increased, whereas the

260 umber of circulating tumor cells in both the E2F1 and E2F2 knockout backgrounds.

261 R-184 was transcriptionally regulated by the E2F1 pathway, which was suppressed in PKP2-deficient cel

262 In response to DNA damage, the E2F1 transcription factor is phosphorylated at serine 31

263 ntified new pro-metastatic functions for the E2F1 target gene Fgf13.

264 Furthermore, the E2F1-ABCG2 axis suppresses chemotherapy-induced cell dea

265 e are also restored to control levels in the E2F1 null background.

266 We show that G9a is present in the E2F1/PCAF complex, and enhances PCAF occupancy and histo

267 Breeding of Kbtbd5 null mouse into the E2F1 null background rescues the lethal phenotype of the

268 PKP2 deficiency leads to suppression of the E2F1 pathway and hypermethylation of the CpG sites at mi

269 ZEB1 and ZEB2, through the mediation of the E2F1 transcription factor; this required Src kinase acti

270 EZH2 expression by enhancing binding of the E2F1 transcriptional activator to the EZH2 promoter.

271 which was downregulated by disruption of the E2F1/DP1 complex.

272 nd DP1 increased without Rb suppression, the E2F1 target genes-including cyclin A, cyclin E, and dihy

273 To test whether the E2F1/DP1 complexes were used for viral transcription, we

274 -ARF prevented MAGE-A11 interaction with the E2F1 oncoprotein and inhibited the MAGE-A11-induced incr

275 To study the role of this E2F1 phosphorylation event in vivo, a knock-in mouse mod

276 KRAS regulated the expression of ILK through E2F1-mediated transcriptional activation, which, in turn

277 Jointly, we propose an intra-adipose tissue E2F1-associated TNFSF paracrine loop engaging lymphocyte

278 ion of BRCA1 promoter by directly binding to E2F1.

279 receptor pathway in which RORalpha binds to E2F1 to inhibit cell cycle progression.

280 e insult, SUMO2 is extensively conjugated to E2F1 mainly at lysine 266 residue, which specifically mo

281 We observed that, in contrast to E2F1 and E2F3, which sensitize to death, E2F4 plays a cr

282 omerase, inhibited cell loss of p21 leads to E2F1- and p53-mediated transcriptional activation of p53

283 Mechanistically, RB loss led to E2F1 cistrome expansion and different binding specificit

284 Moreover, by using siRNA to E2F1, we found that E2F1 was essential for the activity

285 e TopBP1-interacting partner from treslin to E2F1, which results in the termination of replication in

286 ssion profiles of cancer cell lines from two E2F1-driven highly aggressive bladder and breast tumors,

287 of pro-metastatic genes, but also uncovered E2F1 target genes with an unknown role in pulmonary meta

288 nactivation can be partially compensated via E2F1-dependent apoptosis.

289 -matched patients, all obese, whose visceral E2F1 protein expression was either high (E2F1(high)) or

290 Our work proposes a novel paradigm whereby E2F1 plays a key role in the regulation of Trib2 express

291 yclin A-E2F1 pathway that determines whether E2F1 is proliferative or apoptotic in Rb1-deficient tumo

292 ave both uncovered genomic features by which E2F1 regulates metastasis and we have identified new pro

293 In accordance with E2F1 being a negative regulator of DC maturation, C/EBPb

294 estingly, G9a preferentially associates with E2F1 at the G1/S phase and with MyoD at the G2/M phase.

295 east cancer cells revealed a connection with E2F1 and the silencing of SET9 was sufficient to complet

296 d by HER2 signaling are highly enriched with E2F1 binding sites and define a gene signature associate

297 xts due to redundancy of adult function with E2F1 and E2F2.

298 that is responsible for the interaction with E2F1 has a dominant-negative effect on BRCA1 expression

299 es a cell-cycle-independent interaction with E2F1 to recruit enhancer of zeste homolog 2 (EZH2) to di

300 BRCA1 expression by direct interaction with E2F1.

301 metastasis, we interbred MMTV-PyMT mice with E2F1, E2F2, or E2F3 knockout mice.