ライフサイエンスコーパス: retinoblastoma protein

1 and tumor suppressor genes (such as p53 and retinoblastoma protein).

2 CDK4 and induces hypophosphorylation of the retinoblastoma protein.

3 ylation of cyclin-dependent kinase 2 and the retinoblastoma protein.

4 blastoma gene, and lack of expression of the retinoblastoma protein.

5 mainly on binding to Bub1 rather than to the retinoblastoma protein.

6 totic livers leading to lower phosphorylated retinoblastoma protein.

7 ant decrease in the amount of phosphorylated retinoblastoma protein.

8 cells, OGF decreased the phosphorylation of retinoblastoma protein.

9 and CDK4, and reduced phosphorylation of the retinoblastoma protein.

10 for phosphorylation of the tumor suppressor retinoblastoma protein.

11 maintenance deficient 3, and phosphorylated retinoblastoma protein.

12 nduction of cyclin D1 and phosphorylation of retinoblastoma protein.

13 zyme that phosphorylates and inactivates the retinoblastoma protein.

14 iption factors are downstream targets of the retinoblastoma protein.

15 zyme that phosphorylates and inactivates the retinoblastoma protein.

16 Cdk2 and increased levels of phosphorylated retinoblastoma protein.

17 d cleavage and diminished phosphorylation of retinoblastoma protein.

18 ase CDK2 activity and phosphorylation of the retinoblastoma protein.

19 ration in vitro through its interaction with retinoblastoma protein.

20 osphorylation of Ras, ERK, JNK, Akt/PKB, and retinoblastoma protein.

21 noblastoma protein phosphorylation and total retinoblastoma protein.

22 e functions of cellular proteins such as the retinoblastoma protein.

23 ession of cyclin D2, CDK4, CDK6, and phospho-retinoblastoma protein.

24 ly activated by CycE-Cdk2 phosphorylation of retinoblastoma proteins.

25 rest also induced hypophosphorylation of the retinoblastoma protein (6-fold) and induction of p21(WAF

26 but completely abolished phosphorylation of retinoblastoma protein, a cdk2 substrate, indicating tha

27 Additionally, phosphorylation of the retinoblastoma protein, a major regulator of cell cycle

28 sion by phosphorylating and inactivating the retinoblastoma protein, a tumor suppressor that restrain

29 nscription of the B-Myb gene is regulated by retinoblastoma proteins acting directly on the B-Myb pro

30 broblasts by physically associating with the retinoblastoma protein and a p400-TRRAP complex and that

31 ression of cyclin A, hyperphosphorylation of retinoblastoma protein and activation of cyclin-dependen

32 he first barrier, stasis, is mediated by the retinoblastoma protein and can be overcome by loss of p1

33 e process, along with phosphorylation of the retinoblastoma protein and Cdc2 (cell division cycle 2).

34 therefore, increased phosphorylation of the retinoblastoma protein and cell proliferation.

35 s, including increases in hypophosphorylated retinoblastoma protein and concomitant decreases in cycl

36 resulting in inappropriate activation of the retinoblastoma protein and embryonic lethality.

37 ression of Src regulates the activity of the retinoblastoma protein and enhances the differentiation

38 le markers, including phosphorylation of the retinoblastoma protein and lamins, nuclear envelope brea

39 sociated with reduced phosphorylation of the retinoblastoma protein and p27(Kip1) at cdk2 phospho-sit

40 Whereas SV40 LT inactivates the retinoblastoma protein and p53, the contribution of ST i

41 ependent kinase (cdk)-4 to phosphorylate the retinoblastoma protein and release E2F transcription fac

42 Furthermore, hyperphosphorylation of retinoblastoma protein and SMC proliferation were also r

43 program through decreased expression of the retinoblastoma protein and subsequent increased E2F1 exp

44 sociated with the hypophosphorylation of the retinoblastoma protein and the down-regulation of E2F ta

45 rgely prevented the dephosphorylation of the retinoblastoma protein and the induction of p21(WAF1), p

46 of the central cell-cycle regulators CDKN1A, retinoblastoma protein, and cyclin D1 (CCND1), but did n

47 horylation or protein levels of Lck, ERK1/2, retinoblastoma protein, and cyclin D3.

48 cle and that target cyclin-dependent kinase, retinoblastoma protein, and E2F activity all fail to ind

49 n levels, more rapid hyperphosphorylation of retinoblastoma protein, and faster degradation of p27(Ki

50 s oligonucleotides in association with E2F1, retinoblastoma protein, and HDAC2.

51 ion, DNA replication, phosphorylation of the retinoblastoma protein, and induction of minichromosome

52 expression of insulin-like growth factor 2, retinoblastoma protein, and phosphorylated Akt and decre

53 tify and characterize p600, a unique 600-kDa retinoblastoma protein- and calmodulin-binding protein.

54 ively) are suppressed, CDK inhibitor p27 and retinoblastoma protein are activated, E2F1 is sequestere

55 re, we show that replication protein A 2 and retinoblastoma protein are both downstream targets for A

56 mass spectrometry and identified the 600-kDa retinoblastoma protein associated factor, p600, as a cel

57 3',4'-THIF suppressed the phosphorylation of retinoblastoma protein at Ser-795 and Ser-807/Ser-811, w

58 Caffeine inhibited phosphorylation of retinoblastoma protein at Ser780 and Ser807/Ser811, the

59 and p21 resulted in hyperphosphorylation of retinoblastoma protein at serine 780 (p-RB(Ser-780)) fol

60 ncD2 and Rad51 foci require neither Bub1 nor retinoblastoma protein binding.

61 sion of p300 was independent of the Cdk- and retinoblastoma protein-binding domains of cyclin D1.

62 Sequence analysis revealed a retinoblastoma protein-binding motif (LXCXE/D) in the ma

63 ivity through a cyclin-dependent kinase- and retinoblastoma protein-binding-independent mechanism.

64 not Sp1 or Sp4, inhibited phosphorylation of retinoblastoma protein, blocked G0/G1-->S-phase progress

65 p of tumor suppressor proteins including RB (retinoblastoma protein), BRCA1, Ikaros, and CtBP, which

66 RdRp were inhibited by interaction with the retinoblastoma protein but not cyclophilin A.

67 vels of p27(kip1) and hypophosphorylation of retinoblastoma protein but not with decreases in D-type

68 ession was dependent on its interaction with retinoblastoma protein but was independent of its transa

69 HA-p15 decreased the level of phosphorylated retinoblastoma protein by 4.9-fold.

70 romodeoxyuridine, and the phosphorylation of retinoblastoma protein by 40% to 45% in just 2 days, one

71 ly by inhibiting the hyperphosphorylation of retinoblastoma protein by cyclin D1/cdk4.

72 cells in culture through degradation of the retinoblastoma protein by HPV E7 and activation of hTERT

73 OR1 deficiency alters phosphorylation of the retinoblastoma protein by preventing mitogen-induced cyc

74 The retinoblastoma protein C-terminal domain (RbC) is necess

75 AECs promotes proliferation by inhibiting a retinoblastoma protein/c-Abl interaction leading to grea

76 a model in which partial inactivation of the retinoblastoma protein complex leads to the derepression

77 Overexpression of p300 suppressed retinoblastoma protein-dependent gene repression, and th

78 vation of the cyclin/cyclin-dependent kinase-retinoblastoma protein-E2F pathway and prevented the red

79 rotein TAp73 via the cyclin-dependent kinase-retinoblastoma protein-E2F pathway in murine embryonic f

80 vation of the cyclin/cyclin-dependent kinase-retinoblastoma protein-E2F pathway in response to Ang II

81 ecause of the cyclin/cyclin-dependent kinase-retinoblastoma protein-E2F-induced upregulation of pyruv

82 ion of the cyclin D1/cyclin-dependent kinase/retinoblastoma protein/E2F pathway only in TRbeta(PV/PV)

83 preclinical data to support its activity in retinoblastoma protein-expressing tumors.

84 ociated with decreased cyclin-D1 and phospho-retinoblastoma protein expression and increased levels o

85 The retinoblastoma protein family (pRb, p130, p107) plays a

86 n and CDK4/6-related kinase, a member of the retinoblastoma protein family and CDK inhibitors of the

87 endent upon the interaction of HPV16 E7 with retinoblastoma protein family members.

88 Except for the retinoblastoma protein family, Smad3 is the only CDK4 su

89 cellular proteins, including members of the retinoblastoma protein family, the p300/CREB-binding pro

90 tion of DEK expression are controlled by the retinoblastoma protein family.

91 Both GST-OspB and GST-OspF coprecipitated retinoblastoma protein from host cell lysates.

92 protein in a manner which is dependent upon retinoblastoma protein function and have implicated DEK

93 Its protein product, pRB (retinoblastoma protein), functions as a transcriptional

94 The retinoblastoma protein gene RB-1 is mutated in one-third

95 at Ser780 and Ser807/Ser811, the sites where retinoblastoma protein has been reported to be phosphory

96 The LIN-35 retinoblastoma protein homolog and the ubiquitin-conjuga

97 We further show that the retinoblastoma protein homolog LIN-35 and the LIN-13 zin

98 xpression of cyclin D1, D2, and D3 proteins, retinoblastoma protein hyperphosphorylation, and cell cy

99 kinase inhibitor p21(Cip1), which results in retinoblastoma protein hyperphosphorylation.

100 ar Raf and cyclin D1 content that results in retinoblastoma protein hypophosphorylation on amino acid

101 dependent on PKCdelta, whereas induction of retinoblastoma protein hypophosphorylation requires both

102 4a) mRNA and protein expression, and induces retinoblastoma protein hypophosphorylation, thereby trig

103 Although inactivation of the retinoblastoma protein in cells subcultured from the 60-

104 Inactivation of the retinoblastoma protein in quiescent cells through expres

105 ve increased Cdk4 expression that results in retinoblastoma protein inactivation.

106 ll proliferation through CDK4 activation and retinoblastoma protein inactivation.

107 ls in dimethylsulfoxide (DMSO) activates the retinoblastoma protein, increases the proportion of cell

108 n, release of histone deacetylase 1 from the retinoblastoma protein inhibitory complex, and partial a

109 cyclin E-cyclin dependent kinase 2, and the retinoblastoma protein, is closed through a newly identi

110 Therefore, whereas E1A inactivates the retinoblastoma protein, it requires p400 to efficiently

111 pregulation of p27 and hypophoshorylation of retinoblastoma protein, leading to senescence.

112 appears to be responsible for defects in the retinoblastoma protein-mediated transition into S-phase,

113 able to block the hypophosphorylation of the retinoblastoma protein observed upon fenretinide treatme

114 ndependently of its cyclin-dependent kinase, retinoblastoma protein, or p160 (SRC-1) functions in hum

115 ein 7 (MCM7) knockdown in phospho Ser807/811-retinoblastoma protein (p-Rb) defect cells.

116 cells exhibited 16-fold higher levels of the retinoblastoma protein p130/Rb2, which sequesters E2F4 t

117 gene encoding MKlp2 is controlled by the E2F-retinoblastoma protein-p16 pathway, and its widely expre

118 ssion profiles of key cell cycle regulators (retinoblastoma protein, p53, p21(waf1/Cip1), and p16(INK

119 lin A2 by BA treatment resulted in decreased retinoblastoma protein phosphorylation and cell cycle G(

120 clin D1 in vitro led to marked activation of retinoblastoma protein phosphorylation and cell cycle pr

121 ockdown of NOX5 also significantly decreased retinoblastoma protein phosphorylation and increased cel

122 ct that occurred simultaneously with loss of retinoblastoma protein phosphorylation and inhibition of

123 n, perhaps because of its ability to promote retinoblastoma protein phosphorylation and minichromosom

124 cinoma cell lines with CYC202 decreased both retinoblastoma protein phosphorylation and total retinob

125 ism by which CYC202 can cause a reduction in retinoblastoma protein phosphorylation at multiple sites

126 5-overexpressing cells showed an increase in retinoblastoma protein phosphorylation through the forma

127 Finally, the extent of retinoblastoma protein phosphorylation was assayed by We

128 ties in regulation of p130, p27 degradation, retinoblastoma protein phosphorylation, and CDK2 kinase

129 xhibited reduced cell proliferation, reduced retinoblastoma protein phosphorylation, and cyclin-depen

130 r residual cyclin E-cdk2 kinase activity and retinoblastoma protein phosphorylation, followed by prog

131 nhibition of cyclin E-cdk2, and reduction of retinoblastoma protein phosphorylation, limiting endored

132 activation of NF-kappaB, as well as CDK4 and retinoblastoma protein phosphorylation.

133 The retinoblastoma protein pRB and its two homologs p130 and

134 The tumor suppressor function of the retinoblastoma protein pRB is largely dependent upon its

135 The retinoblastoma protein pRb is required for cell-cycle ex

136 The retinoblastoma protein pRB suppresses tumorigenesis larg

137 unit of a holoenyzme that phosphorylates the retinoblastoma protein (pRb) and nuclear respiratory fac

138 The most prominent LT targets are the retinoblastoma protein (pRb) and p53.

139 p CPCs that are initiated by inactivation of retinoblastoma protein (pRb) and related proteins p107 a

140 recruitment of cellular proteins such as the retinoblastoma protein (pRb) and the cyclic-AMP response

141 The retinoblastoma protein (pRB) and the pRB-related p107 an

142 egulated the subcellular distribution of the retinoblastoma protein (pRb) and the protein phosphatase

143 he specific pathways that cooperate with the Retinoblastoma protein (pRB) and the variables that infl

144 g mouse vestibular organs, we identified the retinoblastoma protein (pRb) as a candidate regulator of

145 tumor that develops from loss of functional retinoblastoma protein (pRb) as a result of genetic or e

146 ctivities and reduced phosphorylation of the retinoblastoma protein (pRb) as well as decreased protei

147 In early G1, the retinoblastoma protein (pRB) becomes phosphorylated by c

148 We have previously shown that the retinoblastoma protein (pRb) can activate expression of

149 e segregation, we show that depletion of the retinoblastoma protein (pRB) causes rates of missegregat

150 n-regulation of cyclin D2 and D3 followed by retinoblastoma protein (pRb) dephosphorylation and G(1)

151 s are negatively regulated by members of the retinoblastoma protein (pRb) family.

152 Although the retinoblastoma protein (pRb) has been implicated in the

153 The mechanisms of repression by the retinoblastoma protein (pRB) have been extensively studi

154 e show that nitric oxide (NO) species induce retinoblastoma protein (pRb) hyperphosphorylation and in

155 Expression of the retinoblastoma protein (pRB) in human tumor cells that l

156 of CDK2 activity, and cells arrest with the retinoblastoma protein (pRb) in its hypophosphorylated s

157 en implicated in abrupt dephosphorylation of retinoblastoma protein (pRB) in mitosis, and PP2A, which

158 The function of retinoblastoma protein (pRb) in the regulation of small

159 he SARS-CoV Nsp15 (sNsp15) was stimulated by retinoblastoma protein (pRb) in vitro, and the two prote

160 ulated by E2F transcription factors and that retinoblastoma protein (pRb) inactivation induces Dnmt1.

161 on through the cell cycle is associated with retinoblastoma protein (pRb) inactivation via sequential

162 The retinoblastoma protein (pRb) is a central regulator of t

163 The retinoblastoma protein (pRB) is a critical regulator of

164 1156-1166) describe how the structure of retinoblastoma protein (pRb) is altered by phosphorylati

165 The tumor suppressor function of the retinoblastoma protein (pRb) is historically attributed

166 The retinoblastoma protein (pRB) negatively regulates the pr

167 lecules with significant cellular effects on retinoblastoma protein (pRb) or its related pathways sho

168 alterations of both DNA methylation and the retinoblastoma protein (pRb) pathway found in human canc

169 The retinoblastoma protein (pRb) pathway represents a key co

170 the nucleus and leads to marked increases in retinoblastoma protein (pRb) phosphorylation and cell cy

171 Cyclin/Cdk repression inhibits retinoblastoma protein (pRb) phosphorylation, thereby li

172 Inactivation of previously studied retinoblastoma protein (pRb) targets partially inhibited

173 The retinoblastoma protein (pRb) that is required for osteog

174 We previously demonstrated that loss of the retinoblastoma protein (pRB) tumor suppressor causes cha

175 cal and genetic studies have determined that retinoblastoma protein (pRB) tumor suppressor family mem

176 isplacing E2F transcription factors from the retinoblastoma protein (pRb) tumor suppressor.

177 Here, we present evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-indep

178 In contrast, the phosphorylation status of retinoblastoma protein (pRB) was mediated by mTOR throug

179 ncreased accumulation of hyperphosphorylated retinoblastoma protein (pRb) which coincided with increa

180 show that LIMD1 specifically interacts with retinoblastoma protein (pRB), inhibits E2F-mediated tran

181 cation inhibited hyperphosphorylation of the retinoblastoma protein (pRb), the event that is necessar

182 pendent kinases (cdk) that phosphorylate the retinoblastoma protein (pRb), thereby alleviating repres

183 inase Cdk4 to inhibit phosphorylation of the retinoblastoma protein (pRb), thus blocking the activati

184 ted in an accumulation of hypophosphorylated retinoblastoma protein (pRb), tumor suppressor p53, and

185 Ras also decreases LB1 expression through a retinoblastoma protein (pRb)-dependent mechanism.

186 AP1 binds the E2F1 transcription factor in a retinoblastoma protein (pRb)-independent fashion and inh

187 roteins have been proposed to be involved in retinoblastoma protein (pRB)-mediated repression, but it

188 ng (CREB) binding protein (CBP)/p300 and the retinoblastoma protein (pRb).

189 dicated that A-type lamins interact with the retinoblastoma protein (pRB).

190 te its binding to both class I HDACs and the retinoblastoma protein (pRb).

191 ction in the hyperphosphorylated form of the retinoblastoma protein (pRb).

192 key tumor suppressors, including p53 and the retinoblastoma protein (pRb).

193 ute cell-cycle arrest or inactivation of the retinoblastoma protein (pRb).

194 RBP2 contributed to tumor suppression by the retinoblastoma protein (pRB).

195 ed to the product of the human RB1 gene, the retinoblastoma protein (pRb).

196 The retinoblastoma protein (pRb/p105) tumor suppressor plays

197 g protein (CBP), its paralogue p300, and the retinoblastoma protein (pRb; also called RB1).

198 r of transcriptional corepressors (e.g., the retinoblastoma protein [pRB] and the nuclear hormone cor

199 While the retinoblastoma protein, pRB, alone had no effect on ARHI

200 The retinoblastoma protein, pRb, is positioned at the very e

201 that they are key downstream targets of the retinoblastoma protein, pRB.

202 -specific transcription factor Runx2 and the retinoblastoma protein, pRb.

203 n of the key cell cycle checkpoint regulator retinoblastoma protein, pRb.

204 effect on cyclin D1 and Raf content, altered retinoblastoma protein profile of hypophosphorylation, c

205 horylation of the G1/S transition-regulating retinoblastoma protein Rb at residues Ser795 and Ser807/

206 The retinoblastoma protein Rb has antiproliferative and anti

207 The retinoblastoma protein Rb is critical for the regulation

208 The retinoblastoma protein RB regulates cell proliferation,

209 Impaired retinoblastoma protein RB tumor suppression yields grade

210 OS was not recapitulated by the knockdown of retinoblastoma protein (Rb) and did not require Rb.

211 genic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor pat

212 The retinoblastoma protein (Rb) and the homologous pocket pr

213 d level of cyclin D1, the phosphorylation of retinoblastoma protein (Rb) and the levels of Rb-E2F-reg

214 roliferating and arrested MTC identified the retinoblastoma protein (Rb) as a crucial Cdk5 downstream

215 1, leading to reduced phosphorylation of the retinoblastoma protein (Rb) at Ser(795).

216 a significant decrease in phosphorylation of retinoblastoma protein (RB) at specific sites including

217 inases (CDKs) successively phosphorylate the retinoblastoma protein (RB) at the restriction point in

218 inated by the K1 mutation (E107K) within the retinoblastoma protein (Rb) binding motif of TAg.

219 The retinoblastoma protein (Rb) controls cellular proliferat

220 iously shown that MDM2 binds to and promotes retinoblastoma protein (Rb) degradation.

221 cally infected culture induces Mdm2-mediated retinoblastoma protein (Rb) degradation.

222 ependent kinase (Cdk) phosphorylation of the Retinoblastoma protein (Rb) drives cell proliferation th

223 on by fluorescence in situ hybridization and retinoblastoma protein (RB) expression by immunohistoche

224 ed growth arrest is dephosphorylation of the retinoblastoma protein (Rb) family member p107 by protei

225 The retinoblastoma protein (Rb) family members are essential

226 JCV T125A mutant proteins bind the retinoblastoma protein (RB) family members p107 and p130

227 d model of mammalian cell cycle control, the retinoblastoma protein (Rb) functions to restrict cells

228 Inactivation of the retinoblastoma protein (RB) has a major role in the deve

229 Cdk4, and the rate-limiting tumor suppressor retinoblastoma protein (Rb) have been studied in separat

230 netic modifiers of lin-35/Rb, the C. elegans retinoblastoma protein (Rb) homolog, we have identified

231 egulation of p27, and the maintenance of the retinoblastoma protein (RB) in a hypophosphorylated stat

232 The possible role of retinoblastoma protein (Rb) in the pathogenesis of anapl

233 Recently, ablation of the retinoblastoma protein (Rb) in undifferentiated mouse HC

234 3-dephosphorylated C/EBPalpha interacts with retinoblastoma protein (Rb) independently on E2Fs and se

235 The retinoblastoma protein (Rb) inhibits both cell division

236 Although the retinoblastoma protein (Rb) is known to regulate the gro

237 n-dependent kinase (CDK) inhibitor (CKI)-CDK-retinoblastoma protein (Rb) pathway.

238 d on-treatment lymph node biopsies to assess retinoblastoma protein (Rb) phosphorylation and markers

239 We observed a gradual decrease of Retinoblastoma protein (Rb) phosphorylation and reduced

240 latelet-derived growth factor (PDGF) induced retinoblastoma protein (Rb) phosphorylation in normal hu

241 s of cell-cycle regulatory genes controlling retinoblastoma protein (RB) phosphorylation, and 21% had

242 ccompanied by a dose-dependent inhibition of retinoblastoma protein (Rb) phosphorylation, which funct

243 Inactivation of retinoblastoma protein (Rb) plays a critical role in the

244 The retinoblastoma protein (Rb) plays a pivotal role in regu

245 The tumor suppressor retinoblastoma protein (Rb) plays a pivotal role in the

246 The retinoblastoma protein (Rb) regulates proliferation, cel

247 The tumor suppressor retinoblastoma protein (RB) regulates S-phase cell cycle

248 s were immunoprecipitated and incubated with retinoblastoma protein (Rb) substrate.

249 The retinoblastoma protein (RB) suppresses cell proliferatio

250 Inactivation of the retinoblastoma protein (Rb) through phosphorylation is a

251 te regulation, we examined the role that the retinoblastoma protein (Rb), a central regulator of the

252 We have investigated the role of the retinoblastoma protein (RB), a central regulator of the

253 Here, we acutely ablate the retinoblastoma protein (Rb), a crucial cell cycle regula

254 Whether retinoblastoma protein (RB), a key tumor suppressor and

255 , AHR and E2F1 interact independently of the retinoblastoma protein (RB), because AHR and E2F1 coimmu

256 blocked TGF-beta1-mediated activation of the retinoblastoma protein (RB), decreasing the abundance of

257 levated cyclin D1 levels, phosphorylation of retinoblastoma protein (Rb), motility, invasive properti

258 data demonstrate that JMJ interacts with the retinoblastoma protein (Rb), one of the master regulator

259 ndamental cell cycle proteins, including the retinoblastoma protein (Rb), p53, and MDM2.

260 scripts and protein levels of phosphorylated retinoblastoma protein (Rb), Rb, E2F1, and Cdk4 only in

261 We have observed inactivation of the retinoblastoma protein (Rb), through phosphorylation, in

262 ear antigen 3C (EBNA3C) in regulation of the retinoblastoma protein (Rb), we transfected EBNA3C into

263 Here, we show a novel function for retinoblastoma protein (Rb), where Rb causes sarcomeric

264 cycle reentry and the phosphorylation of the retinoblastoma protein (Rb), whereas in exponentially gr

265 sion resulted in hyperphosphorylation of the retinoblastoma protein (Rb), which correlated with inhib

266 this study, we show that HBZ protein targets retinoblastoma protein (Rb), which is a critical tumor s

267 icits result from hypophosphorylation of the retinoblastoma protein (Rb), which is directly phosphory

268 E1A-induced mRNA response was preponderantly Retinoblastoma protein (Rb)-dependent.

269 though p16(INK4a) is a critical component in retinoblastoma protein (Rb)-mediated growth regulatory p

270 lysine-9 (H3K9) methylation is essential for retinoblastoma protein (RB)-mediated heterochromatin for

271 st and induction of senescence in each of 16 retinoblastoma protein (Rb)-proficient cell lines regard

272 osphorylation and subnuclear localization of retinoblastoma protein (Rb).

273 spase-8-dependent C-terminal cleavage of the retinoblastoma protein (Rb).

274 in the absence of cdk6, to phosphorylate the retinoblastoma protein (Rb).

275 phosphorylation of the cell cycle regulator retinoblastoma protein (Rb).

276 teins followed by hypophosphorylation of the retinoblastoma protein (RB).

277 The retinoblastoma protein (Rb)/E2F pathway links cellular p

278 e1a causes global relocalization of the RB (retinoblastoma) proteins (RB, p130, and p107) and p300/C

279 A fragment of the retinoblastoma protein, Rb(1-400), was used to neutraliz

280 Because the retinoblastoma protein, Rb, plays a central role in the

281 the kinetics of hyperphosphorylation of the retinoblastoma protein, Rb, were analyzed in HCECs from

282 SET (also known as TAF-I or PHAPII) and the retinoblastoma protein, RB.

283 Moreover, cooperation between Mitf and the retinoblastoma protein Rb1 potentiates the ability of Mi

284 PRC2 expression through inactivation of the retinoblastoma proteins RB1 and RBL2.

285 trolled by sequential phosphorylation of the retinoblastoma protein (RB1) by cyclin D-cyclin-dependen

286 ly associates with active hypophosphorylated retinoblastoma protein (Rb1), a known regulator of many

287 Retinoblastoma protein (Rb1), a major tumor suppressor,

288 ase 4 complex, subsequent phosphorylation of retinoblastoma protein, release of histone deacetylase 1

289 modelling of chromatin via interactions with retinoblastoma protein, resulting in diminished inflamma

290 In the nucleus, p600 and retinoblastoma protein seem to act as a chromatin scaffo

291 he Ras/extracellular signal-regulated kinase/retinoblastoma protein signaling pathway, identifying hA

292 is a noncanonical caretaker function of the retinoblastoma protein, such that its deficiency in canc

293 reduced Ki67, c-Myc, and phosphorylation of retinoblastoma protein, suggesting inhibition of the G1-

294 nd cell proliferation through the ability of retinoblastoma protein to repress the transcriptional ac

295 ormation in part by inactivating the p53 and retinoblastoma protein tumor suppressor proteins.

296 on factors are key downstream targets of the retinoblastoma protein tumor suppressor that control cel

297 dramatic decrease in the phosphorylation of retinoblastoma protein was also observed.

298 gained catalytic activity, the G1 gatekeeper retinoblastoma protein was phosphorylated and DNA synthe

299 vated, whereas the level of tumor suppressor retinoblastoma protein was up-regulated in the lungs of

300 effect was seen in cancer cells lacking the retinoblastoma protein, which do not require D-cyclins f

301 In addition, the retinoblastoma protein, which is detectable in the rDNA