ライフサイエンスコーパス: E2F

1 E2F is best known for its role in cell-cycle regulation

2 E2F signaling also interacts with transcriptional progra

3 E2F transcription factor 1 (E2F1) is an important regula

4 E2F transcription factors are important regulators of th

5 E2F transcription factors are known regulators of the ce

6 E2F transcription factors play pivotal roles in controll

7 E2F-1 participates in both cell cycle progression and ap

8 E2F-1 silencing suppressed EP1-mediated FoxC2 and beta1-

9 E2F-2 is a retinoblastoma (Rb)-regulated transcription f

10 E2F-mediated transcriptional repression of cell cycle-de

11 E2Fs are negatively regulated by the retinoblastoma (RB)

12 tions between NF-kappaB and the E2 Factor 1 (E2F-1) and E2 Factor 4 (E2F-4) cell cycle regulators.

13 and the E2 Factor 1 (E2F-1) and E2 Factor 4 (E2F-4) cell cycle regulators.

14 than the mutant U79 promoter with abrogated E2F binding site.

15 n events have distinct effects on activating E2F family members, which suggests a novel mechanism for

16 ignatures, we predicted a role for activator E2F transcription factors in Neu-induced tumors.

17 stinal villi requires at least one activator E2F.

18 thods, we predicted a role for the activator E2F transcription factors in the mouse mammary tumor vir

19 This results in the release of activator E2Fs and induction of E2F-dependent genes.

20 n on RBs results in the release of activator E2Fs and upregulation of E2F target genes; thus, activat

21 genes, but rather by regulation of activator E2Fs or another unidentified mechanism.

22 ocks the transactivation domain of activator E2Fs, inhibiting E2F-dependent transcription and (ii) E2

23 progenitor cells is independent of activator E2Fs, suggests the presence of parallel pathways governi

24 onic fibroblasts is independent of activator E2Fs.

25 d transformation in the absence of activator E2Fs.

26 Current models indicate that activator E2Fs are necessary for cell cycle progression and tumori

27 genics with knockouts of the three activator E2Fs.

28 ulation of E2F target genes; thus, activator E2Fs are considered essential for normal and tumorigenic

29 These results identify COMMD1 and an E2F-metabolic pathway as key regulators of osteoclastoge

30 DREAM contains an E2F, a retinoblastoma (RB)-family protein, and the MuvB

31 We focused on whether E2F4, an E2F member believed to exhibit crucial control over the

32 tokinesis, as induced in erythroblasts in an E2F-2-dependent manner, and we found that CRIK activity

33 oles in cell proliferation, regulation of an E2F-dependent cell-cycle gene expression program, and es

34 Mutations of E-box and E2F consensus sites at the promoter had little effect on

35 luding those encoding the G1/S cyclin D3 and E2F transcription factors and their targets.

36 iferation was mediated through cyclin E1 and E2F-1 in the hearts of the KO mice.

37 on of ASCT2 mRNA and protein expression, and E2F-3 was observed to associate with the ASCT2 promoter.

38 ate specific activator and repressor MYB and E2F transcription factors and indicate the possibility o

39 ent promoted Erk1/2, p38 phosphorylation and E2F-1 expression.

40 e increased level of growth factors, Ras and E2F activity.

41 ogether with phylogenetic analyses of Rb and E2F proteins support the conclusion that Rb evolved spec

42 by p21 controls the retinoblastoma (Rb) and E2F transcription program in an ultrasensitive manner.

43 creases the levels of phosphorylated-Rb1 and E2F-downstream targets, diminishing cell proliferation;

44 The juxtaposition of degron sequences and E2F interaction motifs appears to be a conserved feature

45 otein's activities in growth suppression and E2F transcription factor inhibition.

46 tions with the transcription factors SP1 and E2Fs, which result in the assembly of cell cycle-control

47 Loss of any E2F delayed Neu-induced tumor onset.

48 ed expression of proliferative and apoptotic E2F target genes subsided with gradually reduced roles o

49 r with activation of expression of apoptotic E2F target genes in Skp2(-/-) embryos.

50 We show that while PCL2 and PCL3 are E2F-regulated genes expressed in proliferating cells, PC

51 we reconstruct the regulatory network around E2F, a family of transcription factors whose deregulatio

52 t rapidly along with the presence of E2F4 at E2F-containing B-Myb promoter sites.

53 SKP2 knockdown attenuated E2F-1 and BLM induction.

54 Atypical E2F transcription factors (E2F7 and E2F8) function as ke

55 hematopoietic-specific miR-142 and atypical E2F transcription factors in the regulation of mature T

56 ungus, we find that the Arabidopsis atypical E2F DEL1, a transcriptional repressor known to promote c

57 predicted miR-142 target genes, the atypical E2F transcription factors E2f7 and E2f8, were most highl

58 We genetically inactivated atypical E2Fs in epithelial and mesenchymal neoplasm and analyzed

59 Loss of atypical E2Fs resulted in increased expression of E2F target gene

60 To our surprise, atypical E2Fs suppressed tumor angiogenesis in all three cancer m

61 ether, our studies demonstrate that atypical E2Fs act as tumor suppressors, most likely via transcrip

62 In this study we discovered that atypical E2Fs control tumor angiogenesis, one of the hallmarks of

63 t to previous findings showing that atypical E2Fs promote angiogenesis during fetal development in mi

64 in and skin cancer, the role of the atypical E2Fs, E2F7 and E2F8, in keratinocyte homeostasis, regene

65 cles rescues the lethality of the whole-body E2F-deficient animals.

66 ggest that TAg action on pRBs regulates both E2F-dependent and -independent pathways that govern prol

67 with deregulated cyclin E is not improved by E2F-2-loss, which itself causes reduced peripheral red b

68 e found that these defects are normalized by E2F-2 deletion; however, anemia in mice with deregulated

69 Cell cycle progression is orchestrated by E2F factors.

70 cells and found that E2F1 bound to candidate E2F binding sites in both promoters.

71 sphorylation at three sites known to control E2F/Rb association.

72 We show that MageB2 counteracts E2F inhibition by ribosomal proteins independently of Md

73 oth SBF and its ancestral animal counterpart E2F, which is still maintained in many basal fungi.

74 ed retinoblastoma phosphorylation, decreased E2F activity, and decelerated G1 transition.

75 f loss- and gain-of-function alleles to dial E2F transcriptional output, we have shown that copy numb

76 n activities are mediated by their different E2F transcription factor binding partners.

77 07 CTDs show clear preferences for different E2Fs.

78 LTRAVIOLET-B-INSENSITIVE4 protein and the DP-E2F-Like1 transcriptional repressor, respectively.

79 distribution and localization of Drosophila E2F and dREAM proteins.

80 st that UL97 possesses a mechanism to elicit E2F-dependent gene expression distinct from disruption o

81 However, the inactivation of the entire E2F family in Drosophila is permissive throughout most o

82 additional roles of this pathway, especially E2F transcription factors themselves, in tumor progressi

83 Transcription factor E2F-1 and its interaction with pRb provide a key point o

84 The Rb-controlled transcription factor E2F-3 altered glutamine uptake by direct regulation of A

85 While the E2F transcription factors (E2Fs) have a clearly defined role in cell cycle control,

86 th the use of an integrated system to follow E2F dynamics at the single-cell level and in real time.

87 inoblastoma phosphorylation and allowing for E2F transcriptional activity that accelerates G1- to S-p

88 reveal novel, lineage-specific functions for E2F-2 and suggest that some mitotic kinases have special

89 fatal anemia when a compensatory pathway for E2F-2 production involving insulin-like growth factor-1

90 strate a direct and cell-autonomous role for E2F activators in human cancer.

91 we also identified an unappreciated role for E2F-2 in erythroblast enucleation.

92 We propose novel roles for E2F and ZFP161 in PB-mediated hepatocyte proliferation a

93 frequent, casting doubt on a direct role for E2Fs in driving cancer.

94 We find that e1a displaces RBs from E2F transcription factors and promotes p300 acetylation

95 Drosophila dDP mutants that lack functional E2F/DP complexes.

96 Finally, studies using a Gal4-E2F-1 reporter system show that pRb (R3F) expression red

97 EZH2 promoter through induction of the pRB-->E2F pathway, and (ii) an NF-kappaB p65 driven enhancer i

98 To determine how E2F-2 regulates RBC production, we comprehensively studi

99 However, E2F binds to thousands of genes and, thus, could directl

100 ibiting E2F-dependent transcription and (ii) E2F-bound pocket proteins can recruit chromatin remodeli

101 ular, many DP-1 mutants were found to impair E2F-1-dependent apoptosis.

102 Recent studies implicated E2F in regulation of expression of mitochondria-associat

103 A reduction in E2F binding affinity occurs with S788/S795 phosphorylati

104 y machinery and apoptosis markers, including E2F-1, p21(CIP1), p27(KIP1) and Bcl-2 family proteins.

105 xpression, which inhibits Src, and increased E2F transcription factor 1 expression, which regulates b

106 ration, unscheduled DNA synthesis, increased E2F-responsive genes levels, disrupted differentiation,

107 leading to overexpression through increased E2F binding.

108 bladder cancer is associated with increased E2F and Ezh2 expression and Ezh2-mediated gene expressio

109 With the ablation of individual E2Fs, we noted alterations of tumor latency, histology,

110 SKP2-L248QTAA252, enhanced estrogen-induced E2F-1 and BLM expression.

111 dentified that EP1 agonist treatment induced E2F-1 binding to FoxC2 promotor directly and improved Fo

112 reased expression of key cell cycle inducers E2F transcription factor 1 and cyclin E1.

113 n E-mediated Rb hyperphosphorylation induces E2F transcriptional activator functions.

114 ivation domain of activator E2Fs, inhibiting E2F-dependent transcription and (ii) E2F-bound pocket pr

115 hanisms for how RbC phosphorylation inhibits E2F binding.

116 Investigating E2F target genes that mediate metastasis, we found that

117 by interacting with the DREAM (DP, RB-like, E2F and MuvB) complex at two distinct phases of the cell

118 The DREAM (DP, Retinoblastoma [Rb]-like, E2F, and MuvB) complex controls cellular quiescence by r

119 -FLI1/E2F3 cooperation based on longitudinal E2F target and regulating transcription factor expressio

120 ontaining linear motifs (CKII-acidic, LXCXE, E2F(TD) -like and LXCXE-mimic) predicted to interact wit

121 Targeting the COX-2/EP1/PKC/MAPK/E2F-1/FoxC2/beta1-integrin pathway might represent a new

122 ell invasion in NSCLC by activating the MAPK/E2F-1 signalling pathway.

123 We noted multiple E2F binding site consensus sequences in both promoters.

124 However, the presence of multiple E2F family members complicates our understanding of thei

125 activation increased the expression of MYC-, E2F-, and ribosome-related gene sets, promoted excessive

126 It contains positive and negative E2F proteins and two Cdk inhibitors, and is parameterize

127 bladder cancer, including the activation of E2F transcription factor and subsequent Ezh2 expression

128 e cell cycle, and unrestrained activation of E2F-dependent transcription is considered to be an impor

129 liferation by deregulating the activities of E2F family transcription factors.

130 Pocket proteins regulate the activity of E2F transcription factors during G1-S transition.

131 showed that MageB2 enhances the activity of E2F transcription factors.

132 eveal that crossing a threshold amplitude of E2F accumulation determines cell cycle commitment.

133 at Rb and E2F8 cosuppressed a large array of E2F target genes that are critical for DNA replication a

134 developmental activation requires binding of E2F/DP to a GC-rich motif that facilitates HSF-1 binding

135 dy of evidence has shown that the control of E2F transcription factor activity is critical for determ

136 tasis and therapy resistance.Deregulation of E2F family transcription factors is associated with canc

137 f RbC (RbC(N)) and the marked-box domains of E2F and its heterodimerization partner DP.

138 contribute to the modulation of duration of E2F activation, thereby affecting the pace of cell cycle

139 consequences of the complete elimination of E2F regulation, we profiled the proteome of Drosophila d

140 cal E2Fs resulted in increased expression of E2F target genes, including E2f1.

141 , but has little effect on the expression of E2F target genes.

142 The family of E2F transcription factors is the key downstream target o

143 complexes represent the predominant form of E2F/RBF repressor complexes in Drosophila.

144 These findings identify a key function of E2F in skeletal muscle required for animal viability, an

145 Thus, this novel function of E2F may have a major impact on cell viability, and it is

146 lation of CCNE1 by miR-874 is independent of E2F transcription factors.

147 e release of activator E2Fs and induction of E2F-dependent genes.

148 Proliferation followed the induction of E2F-regulated genes, and depended on factors having stro

149 echanism explaining the observed kinetics of E2F target induction.

150 sults in increased transcriptional levels of E2F target genes.

151 Muscle-specific loss of E2F results in a significant reduction in muscle mass an

152 We report an unexpected mechanism of E2F/DP action that promotes quiescence in this tissue.

153 A.Z.2 controls the transcriptional output of E2F target genes in melanoma cells.

154 Ectopic RB resets the patterns of E2F regulated gene expression in cells derived from tumo

155 Transcriptome profiling of E2F-2-null, mature erythroblasts demonstrated widespread

156 ting chromatin modifiers to the promoters of E2F target genes.

157 on of Aurora B results in down-regulation of E2F-mediated transcription and that the cell cycle arres

158 failed to relieve Rb-mediated repression of E2F reporter constructs.

159 with an increase in autophagy, repression of E2F target genes, and an gene expression signature of bl

160 ino acid), resulting in active repression of E2F target genes.

161 Ewing sarcoma is due to the de-repression of E2F targets as a consequence of transcriptional inductio

162 Cyclin D3 protein, incomplete repression of E2F-mediated gene transcription, and failure to properly

163 escues p107- and p130-mediated repression of E2F-responsive gene expression, but it does not induce t

164 for Rb family protein-mediated repression of E2F-responsive transcription appear to differ for each o

165 ressor is well established as a repressor of E2F-dependent transcription.

166 Rb, this phosphorylation, and the rescue of E2F-responsive transcription, is dependent on the L1 LXC

167 all cell gene signatures identified a set of E2F target genes common between prostate small cell neur

168 Importantly, E2F7/8 repressed a large set of E2F target genes that are highly expressed in human pati

169 ty is not effectuated by active silencing of E2F target genes, but rather by regulation of activator

170 cket domain, which overlaps with the site of E2F transactivation domain binding.

171 the contexts in which a particular subset of E2F targets dictates a biologic outcome.

172 whereby ERalpha/SCF(SKP2) transactivation of E2F-1 feeds forward to drive G1-to-S.

173 1 complex and activates the transcription of E2F-target genes associated with cell cycle progression

174 elease of activator E2Fs and upregulation of E2F target genes; thus, activator E2Fs are considered es

175 Mechanistically, the activation of E2Fs is related to the ability of MageB2 to interact wit

176 coiled-coil and marked-box domains (CMs) of E2Fs.

177 revealed a number of HER2+ subtypes based on E2F activity with differences in relapse-free survival t

178 is independent of these promoter elements or E2F/DP and instead requires a distinct set of tandem can

179 1m mutant virus show no defects in growth or E2F-responsive gene expression because of redundant vira

180 at there was extensive compensation by other E2F family members in the individual knockouts, undersco

181 onditions, and conditions with overexpressed E2F and Cabut, two transcription factor complexes that p

182 7 does not induce the disruption of all p107-E2F or p130-E2F complexes, as it does to Rb-E2F complexe

183 ir phosphorylation and does not disrupt p107-E2F or p130-E2F complexes.

184 nduce the disruption of all p107-E2F or p130-E2F complexes, as it does to Rb-E2F complexes.

185 lation and does not disrupt p107-E2F or p130-E2F complexes.

186 In particular, E2F-2 deletion impairs nuclear condensation, a morpholog

187 ells and suggest that inhibition of the PDGF-E2F-USP1-ID2 axis could serve as a therapeutic strategy

188 y increasing retinoblastoma phosphorylation, E2F-dependent Cdc2 expression and Cdc2-mediated inactiva

189 Given the plethora of potential E2F targets, the major challenge in the field is to iden

190 ressor complex, is directly repressed by pRb/E2F in flies and humans.

191 (KO) caused similar increases in classic pRb/E2F-regulated transcripts in both tissues, but, unexpect

192 In turn, FOG-1 displaces pRb/E2F-2 from GATA-1, ultimately releasing free, proprolife

193 related genes that are direct targets of pRb/E2F proteins.

194 y the E1a oncoprotein, but show preferential E2F binding patterns.

195 letion increased expression of proliferative E2F target genes in the brains of Skp2(+/+) embryos; the

196 ultimately releasing free, proproliferative E2F-2.

197 veals the molecular basis for pocket protein-E2F binding specificity and how cyclin-dependent kinases

198 sential for animal viability since providing E2F function in muscles rescues the lethality of the who

199 ween deregulation of the retinoblastoma (RB)-E2F pathway and the molecular subtype with worse clinica

200 of the shared downstream retinoblastoma (RB)-E2F pathway.

201 Rb-E2F complexes are dissociated and NBE expression is acti

202 oupled with the stochastic dynamics of an Rb-E2F bistable switch, jointly and quantitatively explain

203 ancer and demonstrate the existence of an Rb-E2F-Ezh2 axis in bladder whose disruption can promote tu

204 gene maps for TP53, DREAM, MMB-FOXM1 and RB-E2F and enables prediction and distinction of CC regulat

205 roviding a functional association between RB-E2F dysfunction and altered gene expression in osteosarc

206 ne (RB1) or components regulating the CDK-RB-E2F pathway have been identified in nearly every human m

207 le studies have demonstrated that the CDK-RB-E2F pathway is critical for the control of cell prolifer

208 iously, however, it efficiently disrupted Rb-E2F complexes but failed to relieve Rb-mediated repressi

209 tivation through phosphorylation disrupts Rb-E2F complexes, stimulating transcription.

210 ne expression distinct from disruption of Rb-E2F complexes and dependent upon both the L1 motif of UL

211 Our data indicate that deregulation of RB-E2F pathway alters the epigenetic landscape and biologic

212 The Rb-E2F axis is an important pathway involved in cell-cycle

213 e recent advances in understanding of the RB-E2F pathway in breast cancer.

214 ed cell lines to validate the role of the RB-E2F pathway in regulating the prognostic gene signature.

215 The RB-E2F pathway is altered in many cancers and is also targe

216 , we extended a mathematical model of the Rb-E2F pathway to include members of the microRNA cluster m

217 , and virus-encoded oncogenes disrupt the RB-E2F repressor complexes.

218 -E2F or p130-E2F complexes, as it does to Rb-E2F complexes.

219 naling controls transcription of CHK1 via Rb-E2F by upregulating cyclin D and E.

220 roliferation by activating ERK, mTOR, and Rb/E2F pathways and by increasing glucose uptake and ATP pr

221 The Hippo/Yki and RB/E2F pathways both regulate tissue growth by affecting ce

222 encing of cell cycle regulators including RB/E2F target genes, likely via the permanent removal of H3

223 pression is the result of deregulated P53/RB/E2F pathway activity and is associated with increased pr

224 at a miR-155-mediated perturbation of the RB/E2F axis may play a role in DLBCL pathogenesis, and cont

225 ether, these studies demonstrate that the Rb/E2F cascade directly regulates a major energetic and ana

226 f the cell motility receptor RHAMM by the RB/E2F pathway was critical for epithelial-mesenchymal tran

227 CD4(+) T cells through activation of the Rb/E2F pathway, and that HBZ protein also confers onto CD4(

228 t cyclin D1, an upstream regulator of the Rb/E2F pathway, is an essential component of the ErbB2/Ras

229 HBZ protein interacts with the Rb/E2F-1 complex and activates the transcription of E2F-tar

230 n immunoprecipitation studies for TP53, RB1, E2F, DREAM, B-MYB, FOXM1 and MuvB.

231 al, and biochemical analyses showed that RB1-E2F complexes bind to MPT gene promoters to regulate tra

232 ZBTB33 mediates the cyclin D1/cyclin E1/RB1/E2F pathway, controlling passage through the G1 restrict

233 anism for how Rb may differentially regulate E2F activities.

234 y, NOX4 was induced through p16-Rb-regulated E2F and p22(phox) was induced by Kras(G12V)-activated NF

235 ver, genetic alterations in the RB-regulated E2F family of transcription factors are infrequent, cast

236 rgeted by the ancestral cell cycle regulator E2F, much like extant viral oncogenes.

237 vation of another core cell-cycle regulator, E2F.

238 ion, termed hypo-phosphorylation, to release E2F transcription factors.

239 ession reduces the ability of pRb to repress E2F-1 transcriptional activation, while pRb (R3K) expres

240 while pRb (R3K) expression further represses E2F-1 transcriptional activation relative to that for ce

241 stricts cell cycle progression by repressing E2F-responsive transcription.

242 broadly divided into activator and repressor E2Fs, regulates cell cycle genes.

243 cient stress erythropoiesis in vivo requires E2F-2, and we also identified an unappreciated role for

244 dinated Ubiquitin- Cyclin E- Retinoblastoma- E2F bistable-signalling pathway controlling restriction

245 ation by G1-CDK of Whi5/Rb inhibitors of SBF/E2F transcription factors triggers irreversible S-phase

246 Immunohistochemistry showed E2F-1, FoxC2, and EP1R were all highly expressed in the

247 Specific E2Fs also have prognostic value in breast cancer, indepe

248 We demonstrate that E2F is dispensable for proliferation of muscle progenito

249 genes that mediate metastasis, we found that E2F loss led to decreased levels of vascular endothelial

250 Here we show that E2F family members directly regulate Trib2 in leukemic c

251 Here we show that E2F function in the adult skeletal muscle is essential f

252 We further show that E2F is deregulated during ETI, probably through CKI-medi

253 The E2F family of transcription factors, broadly divided int

254 The E2F transcription factor is a key cell cycle regulator.

255 t a map of the regulatory network around the E2F family, and using gene expression profiles, identify

256 in noncycling cells by complexes between the E2F transcription factors and the retinoblastoma (Rb) tu

257 cell death, which is likely mediated by the E2F transcription factor.

258 ed the viral genome for genes containing the E2F binding site in their promoters.

259 rogression in part by directly disabling the E2F family of cell cycle-promoting transcription factors

260 viral promoter or by promoter mutated in the E2F binding site.

261 The affected genes include the E2F transcription factor family.

262 pressor function primarily by inhibiting the E2F family of transcription factors that govern cell-cyc

263 tion from proliferation to quiescence is the E2F/Rb pathway, whose activity is highly regulated in ph

264 iptional responses, including members of the E2F and RFX families.

265 romoter was dependent on the presence of the E2F binding site.

266 RB works by binding to members of the E2F family of transcription factors and recruiting chrom

267 tions in DP-1 uncouple normal control of the E2F pathway, and thus define a new mechanism that could

268 ongly correlated with high expression of the E2F target and histone methyltransferase gene EZH2.

269 are associated with reduced activity of the E2F target, DNA methyltransferase 1.

270 ed cell cycle progression, expression of the E2F transcription factor 1 (E2F1) and loss of retinoblas

271 ion by binding and inhibiting members of the E2F transcription factor family.

272 GF signaling regulated the expression of the E2F transcription factors, which directly bound to and a

273 derivatives to affect the properties of the E2F-1/DP-1 heterodimer through a transdominant mechanism

274 Rb, pRb (R3F), disrupts the formation of the E2F-1/DP1-pRb complex in cells as well as in an isolated

275 reby inhibiting their ability to repress the E2F-responsive E2F1 promoter.

276 en together, these data demonstrate that the E2F transcription factors are integral to HER2+ tumor de

277 aken together, these results reveal that the E2F transcription factors play key roles in mediating tu

278 e consensus HSE sequence and adjacent to the E2F-binding site at promoters.

279 While the E2F transcription factors (E2Fs) have a clearly defined

280 o the ability of MageB2 to interact with the E2F inhibitor HDAC1.

281 nockouts, underscoring the importance of the E2Fs in HER2/Neu-induced tumors.

282 To genetically test the hypothesis that the E2Fs function to regulate tumor development and metastas

283 ue capacity to bind with high affinity those E2Fs that are the most potent activators of the cell cyc

284 the promoters of G2/M-specific genes and to E2F target genes.

285 fied several key residues that contribute to E2F selectivity in the pocket family.

286 IE regions include motifs that contribute to E2F-DP transcription factor interaction, and consistentl

287 2, SRC3 and RNA polymerase II recruitment to E2F-1 and BLM promoters.

288 Together, E2F and HSF-1 directly regulate a gene network, includin

289 MYB3R3 associates with the repressor-type E2F, E2FC, and the RETINOBLASTOMA RELATED proteins.

290 piAP2 regulators in part because it utilizes E2F/DP1 transcription factors.

291 n analysis between the tumors in the various E2F-mutant backgrounds revealed that there was extensive

292 (RB) regulates S-phase cell cycle entry via E2F transcription factors.

293 during irradiation-induced apoptosis, where E2F-deficient cells are insensitive to cell death despit

294 ential networks suggest a mechanism by which E2F and Cabut regulate distinct gene interactions, while

295 d is to identify specific processes in which E2F plays a functional role and the contexts in which a

296 ases, and protein activity via contacts with E2F transcription partners.

297 e Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and D

298 n and disrupting the interaction of pRb with E2F-1.

299 we show that SBF can regulate promoters with E2F binding sites in budding yeast.

300 tor NF-YA and limits the expression of NF-YA-E2F-coregulated proliferation-promoting genes, PANDA dep