ライフサイエンスコーパス: E2F1

1 E2F1 activity is connected with a variety of cell fates

2 E2F1 binding to the BIRC5 was also enhanced in telomeras

3 E2F1 binds less cyclin A but more target promoters when

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

5 E2F1 is a transcription factor involved in cell prolifer

6 E2F1 is tightly controlled by multiple mechanisms, but w

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

8 E2F1 loss accelerated tumor growth, while E2F2 and E2F3

9 E2F1 regulates ABCG2 expression in multiple cell systems

10 E2F1 targets included glycolysis and metabolic genes inc

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

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

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

14 E2F1-induced cell death is an innate anti-cancer mechani

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

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

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

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

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

20 ccupancy from complexes containing activator E2F1 to complexes containing repressor E2F4, downregulat

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

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

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

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

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

26 Transient transfection of an E2F1 cDNA and 431 bp of the NuSAP promoter demonstrated

27 ction assays demonstrate the formation of an E2F1-E2F7 complex, as well as an E2F7-E2F7 complex on ad

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

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

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

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

32 2A.Z.2-regulated genes are bound by BRD2 and E2F1 in an H2A.Z.2-dependent manner.

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

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

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

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

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

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

39 The finding that pRB and E2F1 cooperate to activate expression of tissue-specific

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

41 ional activator of the androgen receptor and E2F1.

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

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

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

45 g a positive feedback loop between UCH37 and E2F1.

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

47 e, we identify FOXO transcription factors as E2F1 target genes that act in a feed-forward regulatory

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

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

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

51 hemistry showed a strong correlation between E2F1 and NuSAP expression in human prostate cancer sampl

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

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

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

55 Promoter occupation of Alpl and Bglap by E2F1 occurs specifically during activation, and depletio

56 pocyte-specific genes are also cotargeted by E2F1 and pRB during differentiation along their respecti

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

58 ind that E2F7 and E2F8, which are induced by E2F1-3 at G1/S, can form a heterodimer with E2F1 through

59 Mechanistically, promoter occupation by E2F1 and pRB is mutually dependent, and without this coo

60 erexpression appears to be driven in part by E2F1 activation.

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

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

63 breast cancer and is positively regulated by E2F1.

64 les during development and are suppressed by E2F1.

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

66 DNA binding domain) fusions with Orc2, Cdt1, E2F1 or HBO1 coordinated the recruitment of the Mcm7 hel

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

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

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

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

71 nd 431 bp of the NuSAP promoter demonstrated E2F1 as an important regulator of expression.

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

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

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

75 ced by loss of E2F1/Dp function and elevated E2F1/Dp expression suppresses Tara-induced INP different

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

77 We have identified eight endogenous E2F1-binding sites on the Bim promoter using in silico a

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

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

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

81 The transcription factor E2F1 is a key regulator of proliferation and apoptosis b

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

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

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

85 ulation mediated by the transcription factor E2F1, was enhanced by Cry1/Cry2 double mutation.

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

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

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

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

90 acetylase SIRT1 and the transcription factor E2F1.

91 e cell cycle-associated transcription factor E2F1.

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

93 a panel of cell cycle transcription factors (E2F1, E2F4, E2F6, and GABPA) from the Encyclopedia of DN

94 0.9006 for ZFX, 0.8892 for ESRRB, 0.8920 for E2F1.

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

96 o our knowledge, deubiquitinating enzyme for E2F1.

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

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

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

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

101 tly interacts with E2F1, and is required for E2F1 induction of apoptosis and transcription of a numbe

102 sphorylation of this residue is required for E2F1 interaction with CDK8, and that the phosphorylation

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

104 proliferative response including a role for E2F1-3 in the activation of transcription at G1/S and a

105 We identified a signature composed of high E2F1 and low miR-205 expression that promotes resistance

106 nd that a genetic signature composed of high E2F1, low miR-205, and high ERBB3 can render tumor cells

107 However, E2F1 promotes both proliferation and apoptosis.

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

109 nation and linked p107 to hypophosphorylated E2F1 in association with the stabilization and activatio

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

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

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

113 RNAi-mediated silencing of FOXO impaired E2F1 binding to the promoters of cooperative target gene

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

115 cribe that CDK8 phosphorylates serine 375 in E2F1 both in vitro and in cells, and that phosphorylatio

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

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

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

119 3 targets with oncogenic function, including E2F1 and MEF2C, and the predicted miR-223 target, TOX, r

120 tivity of additional oncoproteins, including E2F1 and AKT.

121 1 suppressed cell-cycle regulators including E2F1, E2F2, EXO1, FOXM1, and MCM2.

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

123 The ability of MAGE-A11 to increase E2F1 transcriptional activity was similar to the activit

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

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

126 revents cyclin A from binding and inhibiting E2F1.

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

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

129 of incoherent feedforward loops that involve E2F1, p73/DNp73, and miR-205.

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

131 ndeed targeted by an activator E2F, i.e., is E2F1.

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

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

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

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

136 een to identify candidate genes that mediate E2F1-induced cell death.

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

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

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

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

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

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

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

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

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

146 CF-dependent genes, as well as activation of E2F1-dependent genes.

147 ion with the stabilization and activation of E2F1.

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

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

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

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

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

153 ifically during activation, and depletion of E2F1 severely impairs their induction.

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

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

156 te at nucleotide -246 negated the effects of E2F1 on NuSAP expression.

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

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

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

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

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

162 3 in MF/CTCL lead to increased expression of E2F1, MEF2C, and TOX, which likely contributes to the de

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

164 e for E2F4-8 in repressing the same group of E2F1-3 target genes as cells progress through S phase.

165 This regulation is due to inactivation of E2F1 transcriptional activation, and not to the interfer

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

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

168 classical concept of pRB as an inhibitor of E2F1, but is consistent with the observed roles of these

169 l activation, and not to the interference of E2F1's ability to bind to E2F1-binding sites in various

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

171 Loss of E2F1 alone does not affect tumour susceptibility to MNU,

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

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

174 Furthermore, we show a significant loss of E2F1 recruitment to the promoters of these genes in resp

175 fferentiation can also be induced by loss of E2F1/Dp function and elevated E2F1/Dp expression suppres

176 s 2 (UHRF2) gene as an important mediator of E2F1-induced cell death.

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

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

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

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

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

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

183 thus reflecting the oncogenic properties of E2F1.

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

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

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

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

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

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

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

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

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

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

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

195 romoting transcription factor, we focused on E2F1.

196 tory map developed to summarize knowledge on E2F1 and its interplay with p73/DNp73 and miR-205 in can

197 ibitory effect of growth factor signaling on E2F1-mediated transcription and apoptosis.

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

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

200 hat nuclear extracts of cells overexpressing E2F1 bound directly to the E2F-binding site in the NuSAP

201 B, and reduced levels of its binding partner E2F1.

202 by CDK8 interacting with and phosphorylating E2F1, which acts as a repressor of beta-catenin/TCF tran

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

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

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

206 Thus, pRb-E2F1 is an obesity suppression mechanism in ARC POMC neu

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

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

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

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

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

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

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

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

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

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

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

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

219 1 deacetylates retinoblastoma (Rb) in the Rb/E2F1 complex, leading to dissociation of E2F1 and enhanc

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

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

222 he phosphorylation of S375 by CDK8 regulates E2F1 ability to repress transcription of beta-catenin/TC

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

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

225 rization and its ability to bind and repress E2F1 activities.

226 n is required for TopBP1 to bind and repress E2F1 activity.

227 that CtBP2 is essential for E2F7 to repress E2F1 transcription.

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

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

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

231 21 inhibits RNR2 transcription by repressing E2F1 transcription factor, its transcriptional activator

232 m of tumour suppression by pRb is repressing E2F1.

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

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

235 Specifically, E2F1 negatively regulates both Ogt and Mgea5 expression

236 In support, E2F1 silencing led to the loss of Bim expression in canc

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

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

239 ted HDAC1 from deacetylating and suppressing E2F1.

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

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

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

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

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

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

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

247 We found that E2F1 forms a complex with FOXO1 and FOXO3.

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

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

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

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

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

253 Using the ChIP assay, it was shown that E2F1 directly interacted with the survivin gene (BIRC5)

254 The E2F1 transcription factor is active in many types of sol

255 The E2F1 transcription factor, which is negatively regulated

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

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

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

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

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

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

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

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

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

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

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

267 ession was E2F1-dependent as mutation of the E2F1-binding sites on the Bim promoter inhibited lucifer

268 E-A11 modulated endogenous expression of the E2F1-regulated cyclin-dependent kinase inhibitor p27(Kip

269 lasts are due to decreased activation of the E2F1/Dp transcription factor complex and delayed progres

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

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

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

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

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

275 nown about the molecular circuitry that tips E2F1 balance toward proliferation during normal growth v

276 he interference of E2F1's ability to bind to E2F1-binding sites in various promoters or to interact w

277 ion of BRCA1 promoter by directly binding to E2F1.

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

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

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

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

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

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

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

285 e assay demonstrated that Bim expression was E2F1-dependent as mutation of the E2F1-binding sites on

286 duced oxaliplatin-induced apoptosis, whereas E2F1 downregulation reduced doxorubicin-induced apoptosi

287 s site in an allele-specific manner, whereas E2F1 preferentially bound the risk variant of rs35054928

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

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

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

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

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

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

294 E2F1-3 at G1/S, can form a heterodimer with E2F1 through interactions involving the DNA-binding doma

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

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

297 lation on Ser312 aids p53's interaction with E2F1, and enhances p53-mediated apoptosis.

298 BRCA1 expression by direct interaction with E2F1.

299 rget of E2F, that it directly interacts with E2F1, and is required for E2F1 induction of apoptosis an

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