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

3 CDK4 and induces hypophosphorylation of the retinoblastoma protein.

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

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

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

7 totic livers leading to lower phosphorylated retinoblastoma protein.

8 ant decrease in the amount of phosphorylated retinoblastoma protein.

9 cells, OGF decreased the phosphorylation of retinoblastoma protein.

10 nduction of cyclin D1 and phosphorylation of retinoblastoma protein.

11 for phosphorylation of the tumor suppressor retinoblastoma protein.

12 maintenance deficient 3, and phosphorylated 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 and CDK4, and reduced phosphorylation of the retinoblastoma protein.

20 vely phosphorylates the checkpoint regulator retinoblastoma protein.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 e, such as cyclin-dependent kinases and pRb (retinoblastoma protein), are necessary for efficient mes

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

55 3',4'-THIF suppressed the phosphorylation of retinoblastoma protein at Ser-795 and Ser-807/Ser-811, w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 We found that YM155 rapidly activates the retinoblastoma protein, correlating with the loss of exp

75 and interference with the downstream CDK-Rb (retinoblastoma protein)-E2F signaling pathway.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 4a) mRNA and protein expression, and induces retinoblastoma protein hypophosphorylation, thereby trig

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

101 Inactivation of the retinoblastoma protein in quiescent cells through expres

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

103 ll proliferation through CDK4 activation and retinoblastoma protein inactivation.

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

105 MCV large T up-regulated Sox2 through its retinoblastoma protein-inhibition domain, which in turn

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 ited E2F2 expression and was associated with retinoblastoma protein phosphorylation attenuation, whic

124 5-overexpressing cells showed an increase in retinoblastoma protein phosphorylation through the forma

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

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

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

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

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

130 The retinoblastoma protein pRB and its two homologs p130 and

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

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

133 The retinoblastoma protein pRB suppresses tumorigenesis larg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 1156-1166) describe how the structure of retinoblastoma protein (pRb) is altered by phosphorylati

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

161 The retinoblastoma protein (pRB) negatively regulates the pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 The retinoblastoma protein RB is a tumor suppressor known to

199 The retinoblastoma protein Rb is critical for the regulation

200 The retinoblastoma protein RB regulates cell proliferation,

201 Impaired retinoblastoma protein RB tumor suppression yields grade

202 well-known target of cyclin D-Cdk4,6 is the retinoblastoma protein Rb, which inhibits cell-cycle pro

203 which leads to eventual inactivation of the retinoblastoma protein Rb.

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

205 The Retinoblastoma protein (RB) and DREAM complex (DP, RB-li

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

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

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

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

210 1, leading to reduced phosphorylation of the retinoblastoma protein (Rb) at Ser(795).

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

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

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

214 The retinoblastoma protein (Rb) controls cellular proliferat

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

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

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

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

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

220 The retinoblastoma protein (Rb) family members are essential

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

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

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

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

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

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

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

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

229 3-dephosphorylated C/EBPalpha interacts with retinoblastoma protein (Rb) independently on E2Fs and se

230 The retinoblastoma protein (Rb) inhibits both cell division

231 Retinoblastoma protein (Rb) is a tumor suppressor that b

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

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

234 is frequently disrupted by mutations in the retinoblastoma protein (RB) pathway.

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

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

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

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

239 ssion of several direct p53 targets, reduced retinoblastoma protein (Rb) phosphorylation, and defects

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

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

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

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

244 The retinoblastoma protein (Rb) regulates proliferation, cel

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

246 The retinoblastoma protein (RB) restricts cell cycle gene ex

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

248 The retinoblastoma protein (RB) suppresses cell proliferatio

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

250 ision cycle dilutes the cell cycle inhibitor Retinoblastoma protein (Rb) to trigger division in human

251 AR recruitment of the retinoblastoma protein (Rb) was required to strengthen t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 Intriguingly, we also find that the retinoblastoma protein (RB1) is a direct target of JARID

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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