ライフサイエンスコーパス: E2F-1

1 selective effects in tumors that overexpress E2F-1.

2 feedback control by NTPs that down-regulates E2F-1.

3 rtial activation of the transcription factor E2F-1.

4 ell lines with a tamoxifen-dependent form of E2F-1.

5 or differentiation, including cyclin D1 and E2F-1.

6 hese repressor complexes are displaceable by E2F-1.

7 ase IV is a direct transcriptional target of E2F-1.

8 at is not displaced by the overexpression of E2F-1.

9 -Ras(V12), but not by overexpressed c-Myc or E2F-1.

10 r the observed effects on retinoblastoma and E2F-1.

11 raversal results in persistent expression of E2F-1.

12 he ability of IGF-I to increase synthesis of E2F-1.

13 was markedly reduced in HAECs overexpressing E2F-1.

14 ding of the transcription factors GATA-2 and E2F-1.

15 occur on pRb together with its key effector E2F-1.

16 unctions as a transcription co-repressor for E2F-1.

17 Ebp1 and suppresses its repressive effect on E2F-1.

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

19 e epithelial cells by down-regulating AR and E2F-1.

20 ducibly express the dominant-negative mutant E2F-1 (1-374), expression of the mutant decreased AZ703-

21 d to be important for the down-regulation of E2F-1, -2, and -3A activity after cells have progressed

22 atory machinery, as overexpression of E1a or E2F-1, -2, or -3 overrides the G(1) arrest.

23 dependent kinases, disrupting pRB binding to E2F-1-3, allowing "free" E2F to regulate genes involved

24 E2F-1, a regulator of cell proliferation and viability,

25 As a transcriptional target of E2F-1, a regulator of p53, and an important mediator of

26 b and by cell cycle-dependent alterations in E2F-1 abundance.

27 nisms that underlie the opposing outcomes of E2F-1 activation remain largely unknown.

28 These studies demonstrated that E2F-1 activity at specific promoters is dependent on phy

29 ridol could cause inappropriately persistent E2F-1 activity during S phase traversal and exit.

30 dictate the different biological outcomes of E2F-1 activity have yet to be elucidated.

31 Furthermore, E2F-1 activity is required for flavopiridol-induced apop

32 cyclin A, suggesting that the modulation of E2F-1 activity produced by flavopiridol-mediated cyclin-

33 kinase inhibition, as the residual level of E2F-1 activity that persists may be sufficient to induce

34 Interestingly, elevated E2F-1 activity was sufficient to arrest a substantial su

35 ylation regulates the biological activity of E2F-1 activity, and raise the possibility that arginine

36 nsformed cells, with high baseline levels of E2F-1 activity, may be particularly sensitive to cyclin

37 arks to different functional consequences of E2F-1 activity.

38 rplay that governs the biological outcome of E2F-1 activity.

39 We report here that E2F-1 acts as a direct transcriptional regulator of dual

40 We report here that E2F-1 acts as a transcriptional regulator of MKP-2 (MAPK

41 E2F-1 adenoviral infection of these cells was found to a

42 When combined with Adriamycin or etoposide, E2F-1 adenovirus therapy resulted in an 87% or 91% decre

43 ised in cells homozygous for a nonfunctional E2F-1 allele.

44 nscription factor E2F, and overexpression of E2F-1 allowed proliferation in hypoxic cells, although i

45 clin A-dependent kinase activity neutralizes E2F-1 allowing orderly S phase progression.

46 ions of each drug alone or infection with Ad-E2F-1 alone produced <5% apoptosis by 3 days posttreatme

47 ve effect of PIM-2 was mediated by increased E2F-1 and activated ATM levels.

48 tained in this study place PIM-2 upstream to E2F-1 and ATM in the UV-induced DNA damage response.

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

50 SKP2 knockdown attenuated E2F-1 and BLM induction.

51 2, SRC3 and RNA polymerase II recruitment to E2F-1 and BLM promoters.

52 he ability of IGF-I to increase mass of both E2F-1 and cyclin A but not cyclin E or D1.

53 retinoblastoma and to cause accumulation of E2F-1 and cyclin A.

54 E2F-1 and cyclin B are important regulators of the cell

55 Thus, CD437 modulates the expression of E2F-1 and cyclin B through the simultaneous stimulation

56 1/2 are dephosphorylated in the presence of E2F-1 and DUSP1.

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

58 Conversely, cotreatment with Ad-E2F-1 and low concentrations of etoposide or Adriamycin

59 use of reduced Rb transcription and enhanced E2F-1 and Mad2 expression.

60 or of DUSP1 and that DUSP1 is a link between E2F-1 and MAP kinases.

61 onal analysis of p14(ARF) indicates that the E2F-1 and MDM2 binding domains can be distinguished.

62 findings establish a functional link between E2F-1 and mitogen-activated protein kinases.

63 retinoblastoma, and increased expression of E2F-1 and other 5'-cap-dependent mRNAs, including the G(

64 /AHPN) results in the enhanced expression of E2F-1 and rapid degradation of cyclin B in the absence o

65 BRCA1 assembles with complexes containing E2F-1 and RB to form a repressive multicomponent transcr

66 PRMT5 frequently coincide with low levels of E2F-1 and reflect a poor clinical outcome.

67 cal staining confirmed a marked reduction in E2F-1 and showed induction of apoptosis on terminal deox

68 dUTPase promoter and demonstrate a role for E2F-1 and Sp1 in driving dUTPase expression.

69 d by the combination chemogene therapy of Ad-E2F-1 and topoisomerase II poisons and does not require

70 wild-type cells expressing dominant negative E2F-1 and, instead, stimulated their growth.

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

72 s associated with a dramatic decrease in AR, E2F-1, and cyclin A as determined by Western blot of tis

73 0 up-regulated myocardial expression of Myc, E2F-1, and G1 cyclin-dependent kinase activities, synerg

74 nipulates nuclear factor-kappaB (NF-kappaB), E2F-1, and p73 activity to promote enhanced mitochondria

75 le for the MDM2 x CK1 complex in maintaining E2F-1 anti-apoptotic signaling.

76 mark, and binding of p100-TSN downregulates E2F-1 apoptotic activity.

77 umor cells expressing high levels of ectopic E2F-1 are more sensitive to flavopiridol-induced apoptos

78 phase, with a concomitant decrease in AR and E2F-1 as well as the E2F-1-regulated proteins necessary

79 that modulate the activity and stability of E2F-1, AZ703 treatment induced E2F-1 expression.

80 We also demonstrate that E2F-1 becomes transcriptionally active yet remains assoc

81 that ASA inhibited the transcription factor E2F-1 binding activity to the survivin promoter region,

82 gulation of survivin is due to inhibition of E2F-1 binding activity to the survivin promoter region.

83 ree nuclear factor-kappaB binding sites, one E2F-1 binding site, and one putative inhibition region w

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

85 0 to the TERT promoter resulting in impaired E2F-1 binding, an effect that was dependent on p16.

86 sites, treatment with SAMe could not induce E2F-1-binding activity.

87 contrast to NF-kappaB, although there is an E2F-1-binding site adjacent to the NF-kappaB sites, trea

88 Specifically, E2F-1 binds to a perfect palindromic motif in the MKP-2

89 We found that E2F-1 binds to chromatin encompassing the DUSP1 promoter

90 that deregulated expression of the oncogene E2F-1 blocks the myeloid terminal differentiation progra

91 Levels of E2F-1 bound to Rb also were elevated.

92 nding-deficient BRM-2 mutant interacted with E2F-1 but failed to activate gene expression, our result

93 The silencing of E2F-1 by RNA interference technology restored the functi

94 describe the residue-specific methylation of E2F-1 by the asymmetric dimethylating protein arginine m

95 ing c-myc, transforming growth factor-alpha, E2F-1, c-myc/transforming growth factor-alpha, and c-myc

96 n that adenovirus-mediated overexpression of E2F-1 can efficiently induce apoptosis in cancer cells w

97 y that adenovirus-mediated overexpression of E2F-1 can efficiently induce apoptosis in melanoma cells

98 As a mediator of cell death, E2F-1 can eliminate latent neoplastic cells through apop

99 er to help elucidate the mechanisms by which E2F-1 causes apoptosis.

100 tant cell cycle-related genes like p27, p57, E2F-1, cdc25A, CDK4, cyclin A, cyclin D1, and cyclin E.

101 th dispensable roles of p53, HIF-1alpha, and E2F-1 (classical proteasomal targets that can regulate N

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

103 In contrast to DP-1, however, DP-4/E2F-1 complexes exhibit reduced DNA binding activity.

104 results further suggest a model in which Rb-E2F-1 complexes mediate the anti-apoptotic activity of R

105 In particular, E2F-1 physically binds to an E2F-1 consensus sequence and a palindromic motif in the

106 E2F-1 controls multiple cellular activities through tran

107 lity of IGF-I to activate Cdk2 and to induce E2F-1, cyclin A, and cyclin A-dependent phosphorylation

108 Similarly, BZLF1 increased expression of E2F-1, cyclin E, and stem loop binding protein (SLBP) in

109 genes activated by BZLF1 expression included E2F-1, cyclin E, Cdc25A, and a number of other genes inv

110 s confirmed that BZLF1 induced expression of E2F-1, cyclin E, Cdc25A, and stem loop binding protein (

111 on of Bid can partially restore apoptosis in E2F-1-deficient T cells.

112 hinders methylation by PRMT5, which augments E2F-1-dependent apoptosis, whereas PRMT5-dependent methy

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

114 and functional properties, which impacts on E2F-1-dependent growth control.

115 SP1 levels are significantly increased in an E2F-1-dependent manner following oxidative stress but no

116 e (TERT) through negative cross-talk with an E2F-1-dependent trans-activation of the TERT promoter.

117 Furthermore, DP-4 interferes with E2F-1-dependent transcription and delays cell-cycle prog

118 ese results reveal a crucial role of PAC1 in E2F-1-directed apoptosis.

119 E1A represses c-Myc- and E2F-1-directed transcriptional activation in vivo by seq

120 f downstream target genes reflects increased E2F-1 DNA-binding activity.

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

122 stoma protein is minimally affected, so that E2F-1/DP-1 heterodimers remain bound to DNA.

123 This 16 bp sequence contains a putative E2F-1/DP-1 transcription factor binding site, and this t

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

125 lator of differentiation Egr-1 abrogates the E2F-1-driven block in myeloid terminal differentiation.

126 Using such analysis, E2f-1, E2f-3, p53, and Id2 have been identified as impor

127 E2F-1, the disassociation of E2F-1 from the E2F-1 E3 ligase p45(SKP2), and decreased E2F-1 ubiquitin

128 imulation and inhibition of the cyclin B and E2F-1 E3 ligases, respectively.

129 robes verified that the binding of PARP-1 to E2F-1 enhances binding to the E2F-1 promoter, indicating

130 ) polymerase-1 (PARP-1) in the regulation of E2F-1 expression and promoter activity during S-phase re

131 USP1 is transcriptionally induced by ectopic E2F-1 expression and that extracellular signal-regulated

132 tal counterparts, and high levels of ectopic E2F-1 expression are sufficient to sensitize nontransfor

133 In contrast, BZLF1 did not induce E2F-1 expression in normal human fibroblasts.

134 In the present study, the effect of E2F-1 expression on drug sensitivity of melanoma cells w

135 E2F-1 expression was confirmed by Western blot analysis.

136 stability of E2F-1, AZ703 treatment induced E2F-1 expression.

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

138 eated with a recombinant adenovirus encoding E2F-1 failed to associate with the binding domain of p65

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

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

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

142 acetylation of E2F-1, the disassociation of E2F-1 from the E2F-1 E3 ligase p45(SKP2), and decreased

143 , the retinoblastoma gene product (pRb), and E2F-1 function during cellular proliferation, differenti

144 The mechanisms by which E2F-1 functions in these processes are largely unclear.

145 Our results show that adenovirus-mediated E2F-1 gene transfer can sensitize melanoma cells to some

146 itation experiments with purified PARP-1 and E2F-1, however, revealed that PARP-1 binds to E2F-1 in v

147 In contrast, cyclin A binding to E2F-1 impedes PRMT1 methylation and augments PRMT5 methy

148 mes, and transcription factors (e.g., XBP-1, E2F-1) implicated in MM pathophysiology.

149 sphorylation of RB, and augments the mass of E2F-1 in a time-dependent manner.

150 nscription, indicating the essential role of E2F-1 in mediating their cross-talk.

151 Overexpression of E2F-1 in melanoma cells resulted in two-fold or greater

152 ray assay to identify the genes regulated by E2F-1 in melanoma cells.

153 of the global profile of genes regulated by E2F-1 in melanoma cells.

154 te changes in gene expression in response to E2F-1 in order to help elucidate the mechanisms by which

155 sphatase is a direct transcription target of E2F-1 in signaling apoptosis.

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

157 regulator of p53 and a positive regulator of E2F-1 in undamaged cells.

158 2F-1, however, revealed that PARP-1 binds to E2F-1 in vitro.

159 ficantly, physical association of PARP-1 and E2F-1 in vivo also occurred in wild-type fibroblasts 5 h

160 Experimental overexpression of E2F-1 increased p14(ARF) level and blocked TGF-beta1-ind

161 We show that ectopic E2F-1 increases expression of PAC1 at both transcription

162 We now report that E2F-1 increases the activity of an apoptotic pathway tha

163 bitor (D4476) activated p53 and destabilized E2F-1, indicating that steady-state levels of these prot

164 ding of the biochemical pathways involved in E2F-1-induced apoptosis and possibly to the identificati

165 ve effect against topoisomerase II inhibitor/E2F-1-induced apoptosis and suggests that new protein sy

166 lasts, demonstrate significant resistance to E2F-1-induced apoptosis.

167 e now show that the ability of Rb to inhibit E2F-1-induced cell death is dependent on a functional LX

168 LXCXE protein, cooperates with Rb to inhibit E2F-1-induced cell death.

169 on repression, abrogates the effect of Rb on E2F-1-induced cell death.

170 Rb (retinoblastoma protein) inhibits E2F-1-induced cell death.

171 However, the mechanisms by which E2F-1 induces apoptosis remains poorly understood.

172 The transcription factor E2F-1 induces cell cycle progression at the G1/S checkpo

173 In the present study, we used a tetracycline E2F-1 inducible U2OS osteosarcoma cell line to investiga

174 73, a p53 homologue, have been identified as E2F-1-inducible genes capable of mediating an apoptotic

175 Rather than displacing Rb, excess E2F-1 instead recruits more Rb, leading to direct transc

176 Thus, E2F-1 integrates cell cycle progression with apoptosis.

177 ed levels of cyclin D, and redistribution of E2F-1 into the cytoplasm of motor neurons and glia.

178 Our findings show that E2F-1 is a transcriptional activator of DUSP1 and that D

179 Our findings demonstrate that E2F-1 is a transcriptional activator of MKP-2 and that M

180 Interestingly, E2F-1 is acetylated following oxidative stress.

181 The elevated level of E2F-1 is because of the enhanced stability of the molecu

182 We show here that E2F-1 is directly methylated by PRMT5 (protein arginine

183 Thus, a mechanism for control of E2F-1 is essential, a signal safeguarding against aberra

184 The transcription factor E2F-1 is implicated in the activation of S-phase genes a

185 gments PRMT5 methylation, thus ensuring that E2F-1 is locked into its cell-cycle progression mode.

186 The phosphorylation of E2F-1 is markedly diminished, whereas that of the retino

187 Importantly, E2F-1 is methylated in tumour cells, and a reduced level

188 ly increased following oxidative stress, and E2F-1 is necessary for that induction.

189 We found that E2F-1 is physically associated with the MKP-2 promoter a

190 xplored the hypothesis that new synthesis of E2F-1 is required for insulin-like growth factor-I (IGF-

191 We show that E2F-1 is required for the cellular apoptotic response to

192 acids from within the DNA-binding domain of E2F-1 is sufficient for cell death and that this activit

193 The founding member, E2F-1, is endowed with contradictory activities, being a

194 ession of the p53 homologue p73, a target of E2F-1, is markedly increased by Nutlin-3 in Rb-mutated t

195 A treated KCs were characterized by elevated E2F-1 levels accompanied by accelerated elimination of t

196 In addition, manipulation of E2F-1 levels leads to predictable outcomes when cells ar

197 of p14(ARF) on confluency occurred with low E2F-1 levels.

198 ated this protective effect, irrespective of E2F-1 levels.

199 tination, suggesting CD437 inhibition of E-3 E2F-1 ligase activity.

200 reports show that the transcription factor, E2F-1, may play a role in mediating cytotoxicity of cert

201 t-induced apoptosis and p73 is important for E2F-1-mediated apoptosis induced by Nutlin-3, especially

202 We conclude that an important pathway of E2F-1-mediated apoptosis is dependent on PKR activation

203 due, at least in part, to an increase of the E2F-1-mediated apoptotic cascade.

204 g that PARP-1 acts as a positive cofactor of E2F-1-mediated transcription.

205 Transcription factor E2F-1 mediates apoptosis and suppresses tumorigenesis.

206 E2F-1 mediates apoptosis in the cellular response to oxi

207 Our study demonstrates that E2F-1 mediates apoptosis through transcriptional regulat

208 E2F-1 mediates apoptosis through transcriptional regulat

209 However, the mechanism by which E2F-1 mediates cancer cell killing is largely unknown.

210 c/transforming growth factor-alpha and c-myc/E2F-1 mice, for the 2 categories of human hepatocellular

211 /transforming growth factor-alpha, and c-myc/E2F-1 mice.

212 Finally, we show that this E2F-1/MKP-2 pathway mediates apoptosis under oxidative s

213 on of beta-catenin (exemplified by the c-myc/E2F-1 mouse).

214 ed in cells expressing a nonphosphorylatable E2F-1 mutant incapable of binding cyclin A, suggesting t

215 oquinone suppresses the expression of AR and E2F-1 necessary for proliferation and viability of andro

216 vestigate the effect of increasing levels of E2F-1 on the cytotoxicity of various chemotherapeutic dr

217 (ARF) possesses multiple binding domains for E2F-1, one of which resides within the N-terminal region

218 Whether E2F-1 overexpression exerts potentially antiinflammatory

219 Here we show that adenovirus-mediated E2F-1 overexpression in cancer cells induces expression

220 Therefore, we investigated the effect of E2F-1 overexpression on proteins regulating the G2-M tra

221 ovitine was demonstrated in combination with E2F-1 overexpression, but not to cisplatin, 5-fluorourac

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

223 The E2F-1-PAC1 cascade in cancer cell killing may provide a

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

225 2 is an essential cell death mediator in the E2F-1 pathway.

226 In particular, E2F-1 physically binds to an E2F-1 consensus sequence an

227 E2F-1 physically interacts with the promoter of PAC1, bi

228 ted genes were not known to be responsive to E2F-1 prior to this study.

229 nto S phase, coincident with the increase in E2F-1 promoter activity and expression of E2F-1-responsi

230 mechanism(s) by which PARP-1 may upregulate E2F-1 promoter activity during S-phase re-entry.

231 2fF in vitro and in vivo is dependent on the E2F-1 promoter driving E1A expression in Rb pathway-defe

232 lication were under the control of the human E2F-1 promoter element.

233 The human E2F-1 promoter has been shown to be selectively activate

234 showed that PARP-1 did not directly bind the E2F-1 promoter in a sequence-specific manner.

235 In all of the viruses, the human E2F-1 promoter regulated E1A expression and GM-CSF expre

236 Finally, gel shift analysis with end-blocked E2F-1 promoter sequence probes verified that the binding

237 , respectively) that use the tumor-selective E2F-1 promoter to limit expression of the viral E1A tran

238 g of PARP-1 to E2F-1 enhances binding to the E2F-1 promoter, indicating that PARP-1 acts as a positiv

239 sence of functional E2F binding sites in the E2F-1 promoter, thus linking antitumor viral activity to

240 E2F binding sites in the Ad E2a and cellular E2F-1 promoters and induces both viral and cellular gene

241 Thus, E2F-1 promotes the transcription of Bid, a molecule that

242 The transcription factor E2F-1 promotes vascular smooth muscle cell apoptosis and

243 quent marked downstream decreases in nuclear E2F-1 protein expression and E2F transactivating activit

244 Thus, depleting PRMT5 causes increased E2F-1 protein levels, which coincides with decreased gro

245 Arginine methylation influences E2F-1 protein stability, and the enhanced transcription

246 at the G1/S checkpoint, and deregulation of E2F-1 provokes apoptosis in a wide variety of malignant

247 We constructed an adenovirus (Ad(E2F-1(RC)) so that E1A expression and viral replication

248 Silencing E2F-1 reduced the protective effect of PIM-2, whereas in

249 pertrophic response, while the expression of E2F-1-regulated genes controlling early G1 progression,

250 To further elucidate the consequences of E2F-1-regulated induction of p21, we developed cell line

251 tant decrease in AR and E2F-1 as well as the E2F-1-regulated proteins necessary for cell cycle progre

252 , unsumoylated Ebp1 mutants fail to suppress E2F-1-regulated transcription, resulting in loss of its

253 his model and suggest the mechanism by which E2F-1 regulates hypertrophy.

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

255 in E2F-1 promoter activity and expression of E2F-1-responsive S-phase genes cyclin A and c-Myc.

256 In contrast, overexpression of E2F-1 resulted in a marked increase in sensitivity to vi

257 blocks differentiation at a later stage than E2F-1, resulting in cells that have the characteristics

258 However, analysis of this domain from E2F-1 revealed it does not bind DNA and is consequently

259 e RNA level from the B-myb, cyclin E, cdk-2, E2F-1, ribonucleotide reductase 1, ribonucleotide reduct

260 dent on physiological circumstances and that E2F-1 should be considered a potential target in the tre

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

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

263 Most important, this E2F-1 small interfering RNA also blocks the ability of I

264 As expected, E2F-1 small interfering RNA blocks the ability of IGF-I

265 The enhanced E2F-1 stability is associated with the concomitant acety

266 ident under DNA damage conditions that allow E2F-1 stabilization and give rise to apoptosis.

267 tlin treatments resulted in the same p53 and E2F-1 steady-state protein level changes, indicating tha

268 E2F-1 suppresses extracellular signal-regulated kinase (

269 in-3 in various tumor cells and depletion of E2F-1 suppresses Nutlin-3-induced apoptosis in cells pos

270 stablish that TNFalpha targets IGF-I-induced E2F-1 synthesis, leading to inhibition of the subsequent

271 mulated myoblasts and identified a subset of E2F-1 target genes that are specifically regulated durin

272 We showed that the expression of E2F-1 targets involved in G1/S transit, DNA replication,

273 lex leads to the derepression of a subset of E2F-1 targets necessary for cell growth without division

274 complex leads to derepression of a subset of E2F-1 targets necessary for cell growth without division

275 However, mutants of E2F-1 that lack the transactivation domain are still abl

276 sociated with the concomitant acetylation of E2F-1, the disassociation of E2F-1 from the E2F-1 E3 lig

277 E2F-1, the unique E2F member capable of inducing apoptos

278 Upon overexpression of E2F-1, there was no detectable change in cytotoxicity to

279 merase II inhibitors also cooperated with Ad-E2F-1 to enhance antitumor activity in an in vivo model

280 noprecipitation demonstrated more binding of E2F-1 to pRb in the high expressing IGFBP-rP1/mac25 clon

281 The ability of E2F-1 to prompt apoptosis in DNA damaged cells coincides

282 ation of serines 608/612 inhibits binding of E2F-1 to RB.

283 p21 associates with the E2F-1 transcription factor at the Wnt4 promoter and caus

284 GF-beta1 treatment caused down-regulation of E2F-1 transcription factor resulting in the down-regulat

285 T cells that lack the E2F-1 transcription factor, which is activated as cells

286 at co-regulates the stability of the p53 and E2F-1 transcription factors.

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

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

289 that PARP-1 does not exert a dual effect on E2F-1 transcriptional activation.

290 Taken together, our results demonstrate that E2F-1 transcriptional activity is a critical determinant

291 mediated apoptosis, indicating dependence on E2F-1 transcriptional targets.

292 expression and cell adhesion were reduced in E2F-1-transduced HAECs, associated with a marked decreas

293 The c-myc/E2F-1 tumors were characterized by a high frequency of b

294 the E2F-1 E3 ligase p45(SKP2), and decreased E2F-1 ubiquitination, suggesting CD437 inhibition of E-3

295 Moreover, endogenous E2F-1 upregulates PAC1 and suppresses ERK activity, lead

296 cceptor in poly(ADP-ribosyl)ation reactions, E2F-1 was not poly(ADP-ribosyl)ated by wild-type PARP-1

297 levels of phosphorylated retinoblastoma and E2F-1 were significantly reduced by ER (approximately 40

298 ast, and endothelial cells, which express no E2F-1, were not able to support AdE2F-1(RC) replication.

299 site or the DNA-binding domain equally bind E2F-1, whereas a PARP-1 mutant lacking the automodificat

300 We confirmed direct interaction of E2F-1 with the proximal region of the p21 promoter.