ライフサイエンスコーパス: E2F

1 E2F signaling also interacts with transcriptional progra

2 E2F transcription factors are central regulators of cell

3 E2F transcription factors are important regulators of th

4 E2F transcription factors are known regulators of the ce

5 E2F transcriptional activity is tightly regulated throug

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

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

8 E2F-mediated transcriptional repression of cell cycle-de

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

10 cancer stemness such as, miR-148a, miR-214, E2F family, MYC and SLC7A5.

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

12 retinoblastoma tumor suppressor or activate E2F target gene expression.

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

14 stinal villi requires at least one activator E2F.

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

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

17 onic fibroblasts is independent of activator E2Fs.

18 d transformation in the absence of activator E2Fs.

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

20 reveal a repressor function of the activator E2Fs to restrict the seed maturation programme until the

21 n G2, the degradation of all three activator E2Fs is controlled by cyclin F, the substrate receptor o

22 cilitates recruitment of E2F4 to an adjacent E2F site to promote BRCA1 transcription.

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

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

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

26 a DNA-binding protein that interacts with an E2F site in the BRCA1 promoter where it facilitates recr

27 as increased levels of cyclin D1, A, B1, and E2F, and repression of p21 in an HIF1alpha-dependent man

28 oprotein metabolism, ribosome biogenesis and E2F and MYC transcriptional activities.

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

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

31 ion at the promoters of cell cycle genes and E2F targets upon loss of E2F4 in RB family-mutant cells.

32 rrest, mediated by depletion of MYC/MYCN and E2F transcriptional output, sensitized RAS-driven neurob

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

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

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

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

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

38 switch into a division-competent state, and E2F/Dp1 may promote maintenance of this state.

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

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

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

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

43 ht another mechanism to maintain appropriate E2F protein levels for proper cell growth.

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

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

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

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

48 eins with an emphasis on the newest atypical E2F family members, the specific and redundant functions

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

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

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

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

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

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

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

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

57 uit, highlighting the deep crosstalk between E2F, SCF-Cyclin F, and APC/C in regulating the oscillato

58 ability to increase E2F signaling by binding E2F negative regulator Retinoblastoma-1 (RB).

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

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

61 ive regulators of tumor growth controlled by E2F, MYC, SREBP1 and AKT3 pathways on the one hand, and

62 resistant against chemotherapy and driven by E2F hyper-activation.

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

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

65 Cell cycle progression is orchestrated by E2F factors.

66 tors of this multisubunit repressor complex (E2F-Rb-HDAC) to reverse its suppressive activities and f

67 egulates LEC2, and mutation at the consensus E2F-binding site in the LEC2 promoter de-represses its a

68 in, which recruits the cell-cycle controller E2F on its target genes.

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

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

71 iting cell cycle regulators Cyclin E (cycE), E2F transcription factor 1 (e2f1), and string (stg).

72 l cycle proteins by modulating the Cyclin D1-E2F axes.

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

74 Increasing or decreasing E2F-dependent transcription during S-phase increases or

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 is are members of a family of eight distinct E2F genes encoding transcriptional activators and repres

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

80 athway analyses predicted activation of E2F (E2F transcription factor), DNA damage response, TP53 (tu

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 Early 2 factor (E2F) family transcription factors participate in myriad

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

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

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

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

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

89 V) protein E7 binds to Rb, releasing it from E2F to promote cell cycle progression, and inducing ubiq

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

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

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

93 Using these peptides as a tool to probe host E2F signaling, we show that the disruption of RB complex

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

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

96 these findings reveal a targetable ABL2-HSF1-E2F signaling pathway required for survival by brain-met

97 impairs expression of HSF1 protein and HSF1-E2F transcriptional gene targets.

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

99 erein IL-33 deficiency led to an increase in E2F targets, cell cycle genes, and DNA replication and a

100 We observed that RB had a dominant role in E2F-dependent gene repression during mid to late G1 whil

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

102 n of oncogenic signaling pathways, including E2Fs, Wnt, Myc, and the DNA repair pathway.

103 ve the sequence-specific ability to increase E2F signaling by binding E2F negative regulator Retinobl

104 displayed the same alterations and increased E2F activity.

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

106 leading to overexpression through increased E2F binding.

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

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

109 olved, we found here that HIV-1 Tat inhibits E2F transcription factor 3 (E2F3), CAMP-responsive eleme

110 Here, by studying E2FB-RBR interaction, E2F target gene expression, and epidermal cell number an

111 tion partner (DP), retinoblastoma (RB)-like, E2F and MuvB (DREAM).

112 d protein p130 forms the DREAM (DP, RB-like, E2F, and MuvB) complex and contributes to repression of

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

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

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

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

117 trate the binding of wildtype but not mutant E2F promoters by repressive PRC1.6/E2F6 and DREAM/E2F4 c

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

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

120 ark Pathway analyses predicted activation of E2F (E2F transcription factor), DNA damage response, TP5

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

122 RB complexes ex vivo leads to activation of E2F-driven transcription and increased leukocyte prolife

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

124 In this Review, we discuss the activities of E2F proteins with an emphasis on the newest atypical E2F

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

126 the F-box protein Cyclin F at the center of E2F regulation, demonstrating temporal proteolysis of bo

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

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

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

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

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

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

133 ers, the specific and redundant functions of E2F proteins, how misexpression of E2F transcriptional t

134 Given the importance of E2F transcription factors in mammalian cell cycle regula

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

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

137 echanism explaining the observed kinetics of E2F target induction.

138 sults in increased transcriptional levels of E2F target genes.

139 ancer are associated with elevated levels of E2F targets, high tumor grade, and poor survival.

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

141 In prior work we demonstrated that loss of E2F transcription factors inhibits metastasis.

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

143 ctions of E2F proteins, how misexpression of E2F transcriptional targets promotes cancer and both cur

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

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

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

147 EBPbeta(-/-) DCs showed a down-regulation of E2F cell cycle target genes and associated proliferation

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

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

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

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

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

153 d, together, they support a critical role of E2F signaling for Theileria-induced host cell proliferat

154 ycle regulation, we investigated the role of E2F signaling in Theileria-induced host cell proliferati

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

156 DREAM bind and repress an overlapping set of E2F-dependent gene promoters, it remains unclear whether

157 oteins, but they provide different shades of E2F regulation.

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

159 eading to enhanced expression of a subset of E2F transcription factor family gene targets.

160 kinase inhibitor 2A)-a downstream target of E2F pathway and an activator of TP53-provided a plausibl

161 are enriched for transcriptional targets of E2F, and identified that the androgen receptor (AR) play

162 1 complex and activates the transcription of E2F-target genes associated with cell cycle progression

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

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

165 Whereas control of E2Fs by the retinoblastoma family of proteins is well es

166 l cancers and result in heightened oncogenic E2F activity, leading to uncontrolled proliferation.

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

168 1m mutant virus show no defects in growth or E2F-responsive gene expression because of redundant vira

169 , little is known about DNA repair and other E2F family members.

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

171 7 does not induce the disruption of all p107-E2F or p130-E2F complexes, as it does to Rb-E2F complexe

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

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

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

175 ellular proteins, including histone H3, p53, E2F, and Dnmt1, and is involved in the regulation of gen

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

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

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

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

180 lysis revealed a sustained disruption of pRB-E2F signaling by combination that was accompanied with e

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

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

183 E2F4 often represents the predominant E2F activity in cells.

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

185 ultimately releasing free, proproliferative E2F-2.

186 e downstream CDK-Rb (retinoblastoma protein)-E2F signaling pathway.

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

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

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

190 Rb-E2F/Dp1 regulates G1/S gene expression in animals and la

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

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

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

194 The cyclin-dependent kinase (CDK)-RB-E2F axis forms the core transcriptional machinery drivin

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

196 The Cdk-Rb-E2F pathway integrates external and internal signals to

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

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

199 cket proteins bind to E2F factors forming RB-E2F and DREAM transcriptional repressor complexes.

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

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

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

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

204 gesting interaction between CDKA1 and the Rb-E2F/Dp1 pathways in regulating cell-cycle-specific gene

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

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

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

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

209 istasis analysis indicated that CDKA1 and Rb/E2F/Dp1 regulate multiple fission by distinct mechanisms

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

211 including the Wnt/beta-catenin, YAP/TAZ, RB/E2F, and BET pathways, which converge on key transcripti

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

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

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

215 The Rb/E2F/Dp1 pathway regulates division number as well as com

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

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

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

219 plex SKP-CULLIN-FBXL3 (SCF(FBXL3)) to reduce E2F steady state protein levels.

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

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

222 component, Cryptochrome 2 (CRY2), regulates E2F family members.

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

224 Hyperphosphorylated RB releases E2F transcription factors, activating a transcriptional

225 (Rb) through phosphorylation, which releases E2F transcription factors to drive cell-cycle progressio

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

227 a tumor suppressor that binds and represses E2F transcription factors.

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

229 that DREAM cooperates with RB in repressing E2F-dependent gene expression and cell cycle entry and s

230 is suppressed in normal cells by repressive E2F complexes and that viral or mutational disruption of

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

232 sis of both activator and atypical repressor E2Fs.

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

234 We propose that by restricting E2F activity to the S phase, cyclin F controls one of th

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

236 The same E2F site is required for A3B induction by polyomavirus T

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

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

239 Here we show that a single E2F cis-element mediates repression in normal cells and

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

241 In the short term, E2F mutants unable to bind cyclin F remain stable throug

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

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

244 Here, we show that E2F-dependent transcription, through E2F6, determines th

245 The E2F family of transcription factors, broadly divided int

246 The E2F family of transcriptional regulators sits at the cen

247 The E2F family, classically known for a central role in cell

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

249 The E2F transcription factors and the RETINOBLASTOMA-RELATED

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

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

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

253 le entry and quiescence are regulated by the E2F transcription factors in association with RETINOBLAS

254 The findings denote the E2F/DNA damage response/TP53 axis as a responsible mecha

255 chanisms for this phenotype and identify the E2F regulated genes that coordinate tumor cell metastasi

256 The affected genes include the E2F transcription factor family.

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

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

259 ell lines identified hyper-activation of the E2F cell-cycle master regulator as driver of AR indiffer

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

261 E2F2, and E2F3A, the three activators of the E2F family of transcription factors, are key regulators

262 ranscription factor FOXM1 and members of the E2F family.

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

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

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

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

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

268 xposed DCs exhibited an up-regulation of the E2F transcriptional pathways and an impaired maturation.

269 w we describe the regulatory profiles of the E2F-Rb-HDAC complex together with EBV latent antigens, a

270 stabilization can occur independently of the E2F-regulated MDM2 inhibitor p14(ARF) Here, we report th

271 ith DCM, led to pathogenic activation of the E2F/DNA damage response/TP53 pathway in the heart and in

272 the RB1 gene product, pRB, is to repress the E2F transcription factor family, but pRB also functions

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

274 protein (Rb) was required to strengthen the E2F-Rb transcriptional repression complex.

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

276 Our results show that the E2F-Rb-HDAC complex exhibits similar distributions in ge

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

278 ddition, ZBTB7A was rapidly recruited to the E2F-Rb binding sites by AR and negatively regulated the

279 ZBTB7A is recruited to the E2F-Rb binding sites by AR and negatively regulates the

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 Importantly, these E2F members, in particular activator E2F1 and repressors

283 in the transcriptional suppression of these E2F targets.

284 ivator-type E2FA and E2FB Accordingly, these E2Fs are only partially required for the expression of c

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

286 Thus, E2F-dependent transcription determines the DNA replicati

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

288 hosphorylated state, pocket proteins bind to E2F factors forming RB-E2F and DREAM transcriptional rep

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

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

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

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

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

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

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

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

297 All 14 mP-RBs interact with E2F/DP proteins, but they provide different shades of E2

298 rylation of RB controls its interaction with E2F and inhibits its tumor suppressor properties.

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

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