ライフサイエンスコーパス: E2F2

1 expression, is rescued by miR-24-insensitive E2F2.

2 vivo corneal endothelium that overexpressed E2F2.

3 by either assay in cells that overexpressed E2F2.

4 o redundancy of adult function with E2F1 and E2F2.

5 ress due to dysregulated DNA replication via E2F2.

6 E2A binding site within the first intron of E2F2.

7 data to identify transcriptional targets of E2F2.

8 e targets including the cell cycle regulator E2F2.

9 The E2F2 3'UTR lacks a predicted miR-24 recognition element.

10 E2F2, a related E2F family member that does not induce a

11 The number of TG neurons expressing E2F2, a transcription factor and cell cycle regulator, i

12 ificant effect on tumor progression, loss of E2f2 accelerated lymphomagenesis.

13 et in both oncogenic models, whereas loss of E2f2 accelerated mammary tumorigenesis driven by Myc-ove

14 and promoter-reporter assays indicated that E2F2 activates ECE-1b transcription.

15 ession data supports this hypothesis and low E2F2 activity is associated with a highly unstable tumor

16 liferation is reduced in mice lacking either E2F2 alone or both E2F2 and E2F3a, but not in mice lacki

17 Interestingly, loss of a single copy of E2f2 also accelerated tumorigenesis, albeit to a lesser

18 reas Mip130 (Lin9) (an MMB core protein) and E2f2 (an MMB transcriptional repressor) are not, but are

19 he absence of p19ARF following expression of E2F2, an E2F family member that does not induce apoptosi

20 pRB proteins are inactivated, expression of E2F2 and -3a was increased.

21 shift the A2-protein complexes, whereas anti-E2F2 and 6 antibodies cannot, demonstrating that the A2

22 ults in an increase in affinity for E2F1 and E2F2 and an increase in the ability of p107 to inhibit E

23 ytomatosis viral oncogene homolog) and E2F1, E2F2 and E2F3 (encoding E2F transcription factors 1, 2 a

24 E2F1, E2F2 and E2F3 belong to a subclass of E2F factors though

25 N terminus of E2F1, a domain also present in E2F2 and E2F3 but absent in E2F4 and E2F5, were essentia

26 survival activity, because co-expression of E2F2 and E2F3 does not rescue cells from E2F1-mediated a

27 protein that interacts specifically with the E2F2 and E2F3 family members, dependent on the marked bo

28 E2F1 loss accelerated tumor growth, while E2F2 and E2F3 loss did not.

29 E2F2 and E2F3 mutant backgrounds alleviated Myc prolifer

30 ound and significantly increased in both the E2F2 and E2F3 mutants.

31 E2f alleles we examined the effects of E2f1, E2f2 and E2f3 triple deficiency in murine embryonic stem

32 nding and sequestering E2f activators (E2f1, E2f2 and E2f3), which are invariably portrayed as the ul

33 that at least two other E2F family members, E2F2 and E2F3, are equally capable of inducing S phase.

34 mmunoprecipitation assays, we show that both E2F2 and E2F3, as well as YY1 and RYBP, associate with t

35 ed in mice lacking either E2F2 alone or both E2F2 and E2F3a, but not in mice lacking E2F1.

36 ressing T antigen contain abundant levels of E2F2 and E2F3a.

37 2F DNA binding activity, composed largely of E2F2 and E2F4, and the growth-suppressive E2F4-p130 comp

38 lanoma cells, free E2F DNA binding activity (E2F2 and E2F4, to a lesser extent E2F1, E2F3, and occasi

39 plasmid containing full-length cDNA for both E2F2 and EGFP (pIRES2-E2F2/EGFP).

40 ICC demonstrated the colocalization of E2F2 and EGFP in corneal endothelium with a transfection

41 subunit of the PRC2 complex, as well as the E2F2 and FOXM1 transcriptional networks.

42 E3(-) adenovirus incorporating cDNA encoding E2F2 and green fluorescent protein (GFP) under control o

43 und by a Myb-containing or alternatively, an E2f2 and L(3)mbt form of the complex.

44 lar endothelial growth factor receptor/FLT1, E2F2 and PCM1 oncogenes were highly enriched in ovarian

45 miR-24 directly regulates MYC and E2F2 and some genes that they transactivate.

46 ough the ability of Rb to bind and sequester E2F2 and the ability of E2F8 to compete with E2F2 for E2

47 s a repressor of transcription, dependent on E2F2 and the RBFs.

48 eraction between E2f Transcription Factor 2 (E2f2) and Brain Expressed X-Linked (Bex)/Transcription e

49 several key cell-cycle regulators including E2F2, and chromatin immunoprecipitation assays detected

50 ed expression of SV40 T-antigen (TAg), human E2F2, and dominant negative Sprouty2 (dn-Spry2) genes to

51 uggest that a critical function of the E2F1, E2F2, and E2F3 activators is in the control of a p53-dep

52 rom its general ability to stably bind E2F1, E2F2, and E2F3 and regulate the cell cycle.

53 We now demonstrate that E2f1, E2f2, and E2f3 are also required for oncogene-mediated t

54 We find that E2F1, E2F2, and E2F3 bind to the positive-acting E2F site in t

55 It is widely believed that E2F1, E2F2, and E2F3 can all activate cellular proliferation b

56 rtance of the interactions of pRb with E2F1, E2F2, and E2F3 for cell cycle control.

57 k has shown that the expression of the E2F1, E2F2, and E2F3 gene products is tightly regulated by cel

58 on factor induces transcription of the E2F1, E2F2, and E2F3 genes.

59 ire E2F activator subclass composed of E2f1, E2f2, and E2f3 in mouse embryonic fibroblasts leads to t

60 ated that the targeted inactivation of E2f1, E2f2, and E2f3 results in elevated p21(CIP1) protein lev

61 an cell cycle control, E2f activators (E2f1, E2f2, and E2f3) are portrayed as the ultimate transcript

62 We also show that the E2F activators (E2F1, E2F2, and E2F3) can bind to the survivin promoter and in

63 activators with overlapping functions (E2F1, E2F2, and E2F3) triggered the p53-p21(Cip1) response and

64 F also increased nuclear expression of E2F1, E2F2, and E2F3, consistent with regulation of the G1/S p

65 xpression of the known E2F activators, E2F1, E2F2, and E2F3, the expression of E2F7 is growth-regulat

66 54W) specifically deficient in binding E2F1, E2F2, and E2F3.

67 past experiments, it appears that the E2F1, E2F2, and E2F3a genes are similarly regulated by growth

68 E2F1, E2F2, and E2F3A interact with the cyclin box of cyclin F

69 nto either transcriptional activators (E2F1, E2F2, and E2F3a) or repressors (E2F3b, E2F4, E2F5, E2F6,

70 E2F1, E2F2, and E2F3A, the three activators of the E2F family

71 in the generally repressive Drosophila RBF, E2F2, and Myb (dREAM)/Myb-MuvB complex.

72 r Kruppel-like factor, MEF2C, ETS, NFY, ATF, E2F2, and NRF1 transcription factors in determining tran

73 s induces expression of cyclin D1, E2F1, and E2F2, and promotes proliferation.

74 ore resistant to apoptosis in the absence of E2f2, and the reintroduction of E2F2 into these tumor ce

75 Inactivation of p53 in E2f1-, E2f2-, and E2f3-deficient cells, either by spontaneous m

76 E2f2 -knockout ( E2f2-/- ) and wild-type (WT) mice were fed a choline-def

77 o the regulation of myogenic function, while E2f2 appears to be less important.

78 Furthermore, we demonstrate that E2F1 and E2F2 are transcriptionally induced by DNA damage in an E

79 rs, Mip120 (Myb-interacting protein 120) and E2F2, are required for repression of Gr63a in inappropri

80 y modulates viral replication and identifies E2F2 as a possible target for antiviral therapies.

81 PT inhibitor identified transcription factor E2F2 as the center of a transcriptional hub in the NAD(+

82 th the critical regulator of the cell cycle, E2f2, at a hub.

83 vation of Rb and E2f8 synergizes to increase E2F2 binding to its target gene promoters.

84 E2F2 binding to the Cpt2 promoter was enhanced in DEN-HF

85 in immunoprecipitation assays confirmed that E2F2 binds the ECE-1b promoter, and promoter-reporter as

86 of pRb/p130 upregulated islet expression of E2F2 but not E2F1.

87 Transfection with cyclin D1 or E2F2, but not cyclin E or activated Akt, overcame the ra

88 GR and E2F2, but not E2F1, E2F3a, or E2F3b, cooperatively trans

89 The glucocorticoid receptor (GR) and E2F2, but not E2F1, E2F3a, or E2F3b, cooperatively trans

90 e also led to reduced expression of E2F1 and E2F2, but not E2F4, at the mRNA and protein levels.

91 onizing miR-24 is abrogated by knocking down E2F2, but not MYC, and cell proliferation, inhibited by

92 Expression of either E2F1 or E2F2 can induce postmitotic lens fiber cells to re-enter

93 e of both Myb and Mip130, or of both Myb and E2F2, caused variegated expression in which high or low

94 prominent nodes at genes that enhance (MYC, E2F2, CCNB1, and CDC2) or inhibit (p27Kip1 and VHL) cell

95 Human E2F1 and E2F2 cDNAs were linked to the alphaA-crystallin promoter

96 We utilized in vitro E2F2 ChIP-chip and over expression data to identify tran

97 tingly, real-time quantitative PCR (qPCR) on E2F2 ChIPs indicated that inactivation of Rb and E2f8 sy

98 omic sequences flanking the 5' region of the E2F2 coding sequence.

99 and other data now link together the Myb and E2F2 complexes in higher-order assembly to specific chro

100 Thus, E2F2 converted PC12-derived neurons from a reversible to

101 summary, these findings revealed that GR and E2F2 cooperatively transactivate IEtu1 promoter activity

102 ver, other transcription factors (TFs; e.g., E2F2) could then drive the response, yielding similar ou

103 results indicate that activation of the E2F1-E2F2-CPT2 axis provides a lipid-rich environment require

104 E2f2 deficiency conferred protection against cholestatic

105 E2F2 deficiency protects against MASH and cholestasis, p

106 E2F2 deficiency resulted in increased synthesis and excr

107 feration in a PI3K/Akt/GSK3beta/beta-catenin/E2F2-dependent manner and modulated the cell size increa

108 urthermore, mice deficient for both E2F1 and E2F2 develop nonautoimmune, insulin-dependent diabetes w

109 ombined ablation of E2f1 or E2f3, along with E2f2, did not further accelerate tumorigenesis.

110 In addition, E2F1/E2F2 DKO mice do not recover normal T cell numbers follo

111 in expression of N-Myc target genes ODC1 and E2F2 DOT1L bound to the Myc Box II domain of N-Myc prote

112 E2F1/E2F2 double knockout (DKO) T cells enter S phase in resp

113 from E2F1 knockout (E2F1(-/-)) and E2F1 and E2F2 double knockout (E2F1(-/-)E2F2(-/-)) mice than isog

114 ntly, hematopoietic defects observed in E2F1/E2F2 double-knockout (DKO) mice appear to result from im

115 Importantly, we show that E2F1 and E2F2 double-knockout T cells exhibit more rapid entry in

116 In Drosophila melanogaster the E2f1, E2f2, Dp, and Rbf1 genes all contribute to replication c

117 es are elevated compared to the wild type in E2f2, Dp, and Rbf1 mutant follicle cells.

118 Mutation of E2f2, Dp, or Rbf1 causes ectopic DNA replication through

119 We found that E2F2, DP, RBF1, RBF2, and the Drosophila homolog of LIN-

120 t RBF1 forms complexes with both E2F1/DP and E2F2/DP that cooperate to repress the expression of pre-

121 ularly in the HCCs, of pRb-free E2F1-DP1 and E2F2-DP1 transcription factor heterodimers, as assessed

122 Downstream, E2F2 drives the transcription of members of the inhibito

123 b promoters minimally affects the binding of E2F2, E2F3, E2F4, and E2F5 but significantly inhibits th

124 was specific to E2F1 and was not observed in E2F2, E2F3, or E2F4.

125 on of the entire subset of activators, E2f1, E2f2, E2f3a and E2f3b, singly or in combination in mice.

126 l-length cDNA for both E2F2 and EGFP (pIRES2-E2F2/EGFP).

127 site counters the repression activity of the E2F2 element in young leaves.

128 f2 knockdown in liver, and overexpression of E2f2 elicited opposing effects.

129 in the bone marrow of mice lacking E2F1 and E2F2 exhibit increased cell cycling.

130 ressed cell-cycle regulators including E2F1, E2F2, EXO1, FOXM1, and MCM2.

131 taxel resistance, while miR-522-3p inhibited E2F2 expression and was associated with retinoblastoma p

132 quence that reproduces the normal control of E2F2 expression during a growth stimulation.

133 vels through the use of siRNA confirmed that E2F2 expression facilitated HPV replication but its loss

134 Forced E2F2 expression in the parental cells led to the acquisi

135 e paclitaxel-resistant cells showed stronger E2F2 expression than the parental cells, while E2F2 inhi

136 ling that low miR-522-3p expression and high E2F2 expression were associated with significantly poore

137 h doxycycline significantly reduced ODC1 and E2F2 expression, reduced tumor progression, and improved

138 helial surface was used to image recombinant E2F2 expression.

139 ion, beta-catenin nuclear translocation, and E2F2 expression.

140 In human HCC, E2F1 and E2F2 expressions inversely correlated with CPT2 expressi

141 ylnitrosamine (DEN) administration, E2f1 and E2f2 expressions were increased in NAFLD-related HCC.

142 ype tissue, whereas restoration of Mip130 or E2F2 extinguished Polo expression.

143 E2F2 and the ability of E2F8 to compete with E2F2 for E2f-binding sites on target gene promoters.

144 hopenic conditions, suggesting that E2F1 and E2F2 function redundantly downstream of TCR and/or IL-7

145 These data indicate that E2f2 functions to inhibit widespread genomic DNA synthes

146 rrelated with high levels of MYCN, ODC1, and E2F2 gene expression and independently correlated with p

147 on and N-Myc protein binding at the ODC1 and E2F2 gene promoters and reduced neuroblastoma cell proli

148 n vivo functions of the transcription factor E2F2 have not previously been analyzed or described in t

149 In the absence of E2F1 and E2F2, however, repression of E2F3 elicits profound reduc

150 The identification of a NAMPT-E2F2-ID axis establishes a link between NAD(+) metabolis

151 The loss of E2F1 and E2F2 impedes B-cell differentiation, and hematopoietic p

152 Here, we investigated the potential role of E2F2 in blood pressure regulation.

153 rted a potential oncogenic role for E2F1 and E2F2 in BRAF(wt)/NRAS(wt)/NF1(wt) tumors and a direct li

154 ther this manuscript defines a novel role of E2F2 in cancer progression beyond cell cycle and could i

155 uman datasets to identify conserved roles of E2F2 in human breast cancer through the TCGA breast canc

156 showed that overexpression of either E2F1 or E2F2 in lens fiber cells was sufficient to cause cell cy

157 t drug screening study to define the role of E2F2 in maintaining genomic integrity in breast cancer.

158 We show that the combined loss of E2F1 and E2F2 in mice leads to profound cell-autonomous defects i

159 umorigenesis, and a tumor suppressor role of E2F2 in Myc-mediated mammary tumorigenesis.

160 re we have specifically examined the role of E2F2 in neuronal differentiation using a gain-of-functio

161 Overexpression of the transcription factor E2F2 in nonmitotic human corneal endothelial cells resul

162 Overexpression of the transcription factor E2F2 in nonproliferating rabbit corneal endothelial cell

163 The effects of miR-522-3p and E2F2 in ovarian cancer were examined using public databa

164 ive and memory T cells lacking both E2F1 and E2F2 in response to lymphopenic conditions, suggesting t

165 results indicate specific roles for E2F1 and E2F2 in the induction of E2F target genes, which contrib

166 ed with controls, implying a direct role for E2F2 in transcriptional repression.

167 C) localization tested for overexpression of E2F2 in transfected corneal endothelial cells and permit

168 Liver-specific induction of E2F2 in vivo hampered the transcriptional program involv

169 Endogenous E2F2 increased in PC12 cells in response to nerve growth

170 vealed that it proceeded in a p53, E2F1, and E2F2-independent manner.

171 increase in a PI3K/Akt/GSK3beta/beta-catenin/E2F2-independent manner.

172 or potentiated (ex vivo) by loss of E2F1 and E2F2, indicating divergent requirements for these E2F fa

173 Tceal8 both preserved cell viability during E2f2-induced cell cycle re-entry.

174 Although Tceal8 inhibited E2f2-induced S-phase re-entry, Bex1 facilitated DNA synt

175 entry upon NGF removal, forced expression of E2F2 inhibited these events and induced apoptosis.

176 F2 expression than the parental cells, while E2F2 inhibition sensitized the resistant cells to paclit

177 In contrast, neither E2F1 nor E2F2 interacted with the p68 promoter under these condit

178 e absence of E2f2, and the reintroduction of E2F2 into these tumor cells resulted in an increase of a

179 Therefore, E2F2 is a critical miR-24 target.

180 Here, we investigated whether E2F2 is involved in MASLD-associated cholestasis and, if

181 Accordingly, we demonstrate E2F2 is required for GSC self-renewal.

182 We show that loss of E2f2 is viable, but causes partial female sterility asso

183 (PCNA) and showed that the proximal element (E2F2) is required for the full repression of PCNA expres

184 These results were recapitulated following E2f2 knockdown in liver, and overexpression of E2f2 elic

185 xpression data from tumors revealed that the E2F2 knockout background resulted in fewer tumors with E

186 circulating tumor cells in both the E2F1 and E2F2 knockout backgrounds.

187 ata was integrated with gene expression from E2F2 knockout tumors in an MMTV-Neu background.

188 reduction in circulating tumor cells in the E2F2 knockout.

189 E2f2 -knockout ( E2f2-/- ) and wild-type (WT) mice were

190 Furthermore, loss or downregulation of E2F2 led to a decline in ECE-1b levels, to higher levels

191 Reduction of E2F2 levels through the use of siRNA confirmed that E2F2

192 In human NAFLD, E2F1 and E2F2 levels were also increased and positively correlate

193 n and outgrowth were markedly inhibited when E2F2 levels were reduced.

194 These results identify the E2f2 locus as a tumor suppressor through its ability to

195 dependent activation and modification of the E2f2 locus is required for cell cycle progression preced

196 These results indicate that E2F2 may have a unique role in maintaining the postmitot

197 GR and E2F2 mediate cooperative transactivation of IEtu1 promot

198 hroid terminal differentiation by preventing E2F2-mediated aberrant transcriptional activation throug

199 pathways and upregulation of the FOXM1- and E2F2-mediated cell cycle transitions, as well as epigene

200 hromatin immunoprecipitation), and repressed E2F2-mediated ECE-1b promoter activity (promoter-reporte

201 Administration of DEN-HFD in E2f1 (-/-) and E2f2 (-/-) mice enhanced fatty acid oxidation (FAO) and

202 E2f1 (-/-) and E2f2 (-/-) mice were resistant to DEN-HFD-induced hepato

203 and in ex vivo ring assays, aortas from the E2F2(-/-) mice exhibited significantly greater contracti

204 e ECE-1 isoform, were significantly lower in E2F2(-/-) mice than in wild-type mice.

205 ures were significantly higher in E2F2-null (E2F2(-/-)) mice than in their wild-type littermates, and

206 and E2F1 and E2F2 double knockout (E2F1(-/-)E2F2(-/-)) mice than isogenic wild-type MEFs.

207 The protective effects observed in E2f2-/- mice were lost when a miR-34a-5p mimic was used.

208 lated miR-34a-5p, which was downregulated in E2f2-/- mice.

209 etic system that is also defective in E2f1-/-E2f2-/-mice The demonstration that beta cell maintenance

210 row can prevent or rescue diabetes in E2f1-/-E2f2-/-mice.

211 ex was sensitive to the dose of the subunits E2F2, Mip120, Caf1, and Lin-52 but not Mip130 or Mip40.

212 tance in vitro through the downregulation of E2F2; miR-522-3p supplementation may be a therapeutic ta

213 ns of metabolic genes enriched with EGR1 and E2F2 motifs, whose transcriptional levels were significa

214 E2f2 mRNA and protein levels were markedly decreased in

215 E2f2 mutant females display a 50% reduction in chorion g

216 The ectopic genomic replication of E2f2 mutant follicle cells can be suppressed by reducing

217 RT-PCR analyses of RNA purified from E2f2 mutant follicle cells indicate an increase in the l

218 E2f2 mutant follicle cells terminate endocycles on sched

219 Consistent with these observations, E2F1/E2F2 mutant mice are highly predisposed to the developme

220 Pancreatic exocrine cells in E2f1-/-E2f2 mutant mice become increasingly polyploid with age,

221 E2F2 mutant mice show erythroid maturation defects that

222 E2f1/E2f2 mutant mice transplanted with wild-type, but not ma

223 roughout the entire follicle cell nucleus in E2f2 mutants, consistent with their use at many genomic

224 ntent in both Rbf1 and Dp mutants but not in E2f2 mutants.

225 onal derepression is greater in Rbf1 than in E2f2 mutants.

226 2 mutants was indistinguishable from that of E2F2 mutants.

227 As reported previously for the E2F2 mutation, the E2F1 and E2F1+2 mutations partially r

228 In fact, miR-24 regulates expression of E2F2, MYC, AURKB, CCNA2, CDC2, CDK4, and FEN1 by recogni

229 es with N-Myc and BRD4, and is important for E2F2, N-Myc and c-Myc transcription.

230 panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitr

231 omised in E2f1 null mice but not affected in E2f2 null mice.

232 blood pressures were significantly higher in E2F2-null (E2F2(-/-)) mice than in their wild-type litte

233 in immunoprecipitation studies revealed that E2F2 occupied IEtu1 promoter sequences when the BoHV-1 g

234 Finally, Sam68 coimmunoprecipitated with E2F2, occupied the ECE-1b promoter (chromatin immunoprec

235 in immunoprecipitation studies revealed that E2F2 occupies IEtu1 promoter sequences in cultured cells

236 ty of RYBP to mediate an interaction between E2F2 or E2F3 and YY1 is an important component of Cdc6 a

237 S phase is impaired in the absence of either E2F2 or E2F3 but not E2F1 or E2F4.

238 Depletion of 14-3-3 tau or E2F1, but not E2F2 or E2F3, blocks adriamycin-induced apoptosis.

239 on, YY1 and RYBP, in combination with either E2F2 or E2F3, can stimulate Cdc6 promoter activity syner

240 nd represses the activities of E2F1, but not E2F2 or E2F3.

241 ly reduced in cells deleted for E2F1 but not E2F2 or E2F3.

242 asis, we interbred MMTV-PyMT mice with E2F1, E2F2, or E2F3 knockout mice.

243 umor progression in mice deficient for E2f1, E2f2, or E2f3.

244 p14(ARF) promotes p53 activity, and E2F2 overexpression in p53 wild-type cells normally lead

245 Moreover, the relative action of RB versus E2F2 overexpression on specific genes demonstrates that

246 phosphorylation (PSM-RB) when compared with E2F2 overproduction.

247 st cancer we found that a low probability of E2F2 pathway activation was associated with increased re

248 Thus, E2F1 and E2F2 play essential and redundant roles in the proper co

249 Furthermore, T cells lacking E2F1 and E2F2 proliferate much more extensively in response to su

250 demonstrated EKLF occupancy at the proximal E2f2 promoter in vivo.

251 ells, E7 acts to inhibit HDAC binding to the E2F2 promoter resulting in activation of expression.

252 hromatin modifier, EKLF binding sites in the E2f2 promoter were located in a region of EKLF-dependent

253 ells, similar to the control of the E2F1 and E2F2 promoters.

254 s, a Tax-associated increase in steady-state E2F2 protein was also documented.

255 se microRNAs reduced the levels of c-Myc and E2F2 proteins.

256 E2F2, RBF, and Mip130/LIN-9 acted in opposition to Myb b

257 of gene expression by Myb, Mip130/LIN-9, and E2F2-RBF in vivo, and also provide an explanation for th

258 Collectively, we demonstrate that IFI6, via E2F2 regulates DNA replication and melanoma development

259 a cell-cycle-independent mechanism by which E2F2 regulates endothelial function, arterial contractil

260 idating in this context that upregulation of E2F2 represents a key intermediate event in a HER2 oncog

261 In contrast, E2F1 and E2F2 repressors function redundantly for some genes in t

262 Remarkably, inactivation of E2f2 rescued the erythropoietic defects resulting from R

263 Compared with the control, transduction with E2F2 resulted in progression from the G(1) to the S phas

264 We show that the combined loss of E2F1 and E2F2 results in profound effects on hematopoietic cell p

265 t overexpression of the transcription factor E2F2 results in replication in nonproliferating human co

266 ls in S phase, the combined loss of E2F1 and E2F2 results in significantly decreased expression and a

267 kingly, it was observed that loss of E2F1 or E2F2 significantly reduced the metastatic capacity of th

268 element (E2F1) and how it interacts with the E2F2 site to regulate the PCNA promoter.

269 In human breast cancer E2F2, status was also correlated with a patient's respon

270 E2F1 or E2F2 stimulated bICP0 early promoter activity at least 1

271 cient for the transcription factors E2F1 and E2F2 suffer from a chronic pancreatitis-like syndrome an

272 he absence of other E2F activators, E2f1 and E2f2, suggesting that these isoforms have redundant func

273 Absence of the dREAM subunit Mip130 or E2F2 suppressed the Myb-null cytokinesis defect.

274 ntly infected calves increased the number of E2F2(+) TG neurons.

275 3-fold increase) in cells that overexpressed E2F2 than in control samples.

276 elative functional contributions of E2F1 and E2F2 to gene expression and cell cycle control depends o

277 ntribution of transcription factors E2F1 and E2F2 to NAFLD-related HCC and their involvement in metab

278 is induction is the ability of E2F1, and not E2F2, to upregulate Chk2 expression.

279 n increase in the ability of p107 to inhibit E2F2 transactivation.

280 roto-oncogene, upregulates expression of the E2F2 transcription factor.

281 These findings identify E2F1 and E2F2 transcription factors as metabolic drivers of hepat

282 r studies of mice deficient for the E2F1 and E2F2 transcription factors have revealed essential roles

283 E7 was found to specifically activate E2F2 transcription in suprabasal keratinocytes through i

284 The Drosophila Myb oncoprotein, the E2F2 transcriptional repressor, and the RBF and Mip130/L

285 Through these methods we predict that E2F2 transcriptionally regulates mediators of DNA repair

286 y (E)15.5, strong expression of the E2F1 and E2F2 transgenes was detected in lens fiber cells with li

287 downstream of the GREs was transactivated by E2F2 unless two adjacent Sp1 binding sites were mutated.

288 At many of these sites, E2F2 was critical for repression, whereas at other nonov

289 E2F2 was overexpressed in the liver by AAV8.

290 Expression of either E2F1 or E2F2 was sufficient to induce the transcription of cycli

291 majority of these genes, including E2f1 and E2f2, was abolished in muscles lacking satellite cell ac

292 The E2F3a increase, but not that of E2F2, was dependent on E2F1.

293 the E2F transcription factor family (E2f and E2f2), which controls the expression of genes that regul

294 ession signature--including STAT1, CD74, and E2F2--which strongly correlates with the magnitude of th

295 Using PCR arrays, we focused on E2F2, with the luciferase reporter assay revealing that