ライフサイエンスコーパス: pRb

1 inactivation of the retinoblastoma protein (pRb).

2 mors showed sustained or increased levels of pRB.

3 duced CIN in cancer cells lacking functional pRB.

4 and inactivation of the cell cycle inhibitor pRb.

5 E motif that is crucial for interaction with pRb.

6 nsformative pathways, including both p53 and pRb.

7 via its influence on the pocket protein (PP) pRb.

8 as well as the interaction between BRG1 and pRB.

9 selected patients with contraindications to PRB.

10 pled to R5020-dependent turnovers of PRA and PRB.

11 feasible and appears to be safe compared to PRB.

12 odeling factor that interacts with BRCA1 and pRB.

13 ruses that encode a protein to interact with pRb.

14 ession from a promoter normally repressed by pRb.

15 to be the principle process regulated by Akt-PRB.

16 and p21, and activation failure of Cdc2 and pRb.

17 , and increased expression of p16(INK4a) and pRB.

18 ative to that for cells expressing wild-type pRb.

19 anism involving inactivation of both p53 and pRb.

20 activation of the tumor suppressors, such as pRb.

21 ho were considered unsuitable candidates for PRB (4.2% of all renal transplant biopsies at our instit

22 n of full-length HPV16 E7 promotes increased pRb acetylation and that this response depends both on t

23 e molecular signals leading to cyclin D/Cdk4/pRb activation following ischemic insult are presently n

24 leagues demonstrate that persistent CDK4 and pRB activation underlie acquired resistance to phosphati

25 Effects of pRB activation/inactivation on glutamine catabolism were

26 moter binding factor target genes and allows pRb activity to be effectively integrated with the DNA d

27 rate that the upstream-downstream linkage of PRB affects the speciation and mobility of As in downstr

28 Increasing evidence suggests that pRb also promotes differentiation, but the mechanisms ar

29 alogue p300, and the retinoblastoma protein (pRb; also called RB1).

30 tion of the retinoblastoma tumor suppressor (pRB) alters the expression of a myriad of genes.

31 n the cytoplasm, decreased overall levels of pRb, an increased proportion of cells in the S phase of

32 multaneous use of nitrate and perchlorate by PRB and competition for H(2), the same resources in PRB,

33 istance to CDK4/6 inhibitors such as loss of pRb and cyclin E1 overexpression also exhibited decrease

34 ld constitute a remarkable situation wherein pRB and E2F would be cotargeting genes for activation.

35 The finding that pRB and E2F1 cooperate to activate expression of tissue-

36 ility of mice deficient in the expression of pRb and either of two related "pocket" proteins, p107 an

37 ived from pRb-negative tumors do not express pRb and express the neuroendocrine tumor markers synapto

38 This study reveals that pRb and its interaction with Nsp15 can affect coronaviru

39 t by binding and inducing the degradation of pRb and its related pocket protein family members, p107

40 The retinoblastoma protein pRB and its two homologs p130 and p107 form the family o

41 We conclude that pRb and p107 act together to efficiently suppress head a

42 These results reveal an overlapping role for pRB and p107 in cartilage development, endochondral ossi

43 These results reveal an overlapping role for pRB and p107 in cartilage development, endochondral ossi

44 Mice deficient for pRb and p130 in their head and neck epithelia showed int

45 s, due to compensatory tumor barriers in p16-pRB and p19-p53-p21 axes.

46 action with several host proteins, including pRb and p300/CBP.

47 correlate with the combined inactivation of pRB and p53 and that this association is evident in two

48 When pRb and p53 are genetically inactivated, cells irreparab

49 itumor mechanisms that remain effective when pRb and p53 are genetically inactivated.

50 nconventional cancer cell vulnerability when pRb and p53 are inactivated.

51 pRb and p53 are the two major tumor suppressors.

52 pRb and p53 are two major tumor suppressors.

53 Here we identify pRb and p53 doubly deficient (DKO) prostate tumorigenesi

54 A similar synergy between pRB and p53 inactivation was observed in HCT116 cells.

55 e cooperative effect of inactivation of both pRB and p53 tumor suppressor pathways that promotes CIN.

56 In the absence of pRb and p53, p27 was unable to inhibit DNA synthesis in

57 sferase domain of CBP/p300 into proximity to pRb and promoting acetylation, leading to disruption of

58 r, our results show that perturbed Lap2alpha/pRb and Smad2/3 signaling are important regulatory pathw

59 t phosphorylates the retinoblastoma protein (pRb) and nuclear respiratory factor (NRF1) proteins.

60 proteins such as the retinoblastoma protein (pRb) and the cyclic-AMP response element binding binding

61 acteria (DB), perchlorate-reducing bacteria (PRB), and sulfate-reducing bacteria (SRB), responded to

62 eceptor (PR) exists in two isoforms, PRA and PRB, and both contain activation functions AF-1 and AF-2

63 stitutive expression of E6, Cyclin D1, CDK4, pRb, and Rb and induced the protein levels of p21 and p2

64 competition for H(2), the same resources in PRB, and space in a biofilm.

65 s, pyrosequencing illustrated that while DB, PRB, and SRB responded predictably to changes in accepto

66 gas-phase polarizations for (129)Xe and Rb (PRb approximately 96%).

67 adigm distinct from the classical concept of pRB as an inhibitor of E2F1, but is consistent with the

68 T1 leading to increased levels of acetylated pRb as well as acetylated H4K16 both globally and at tel

69 m loss of functional retinoblastoma protein (pRb) as a result of genetic or epigenetic changes that a

70 Because PRB, as well as PRA, coimmunoprecipitated with FAK, both

71 While perchlorate-reducing bacteria (PRB), assayed by qPCR targeting the pcrA gene, remained

72 PRMT4 specifically methylates pRb at the pRb C-terminal domain (pRb C(term)) on argini

73 to expression of a truncated LT that retains pRB binding but with a deletion of the C-terminal domain

74 Mutations in the pRb-binding motif rendered sNsp15 to be differentially m

75 DNA binding, transcriptional activation and pRb-binding properties of the heterodimer.

76 Moreover, unliganded PRB but not PRA enhanced FAK Tyr397 phosphorylation and

77 Surprisingly, unliganded PRB but not PRA strongly enhanced cell migration as comp

78 Ewing sarcoma we report replacement of E2F3/pRB by constitutively expressed repressive E2F4/p130 com

79 mer mediates an interaction between TAZ2 and pRb by promoting formation of a ternary complex.

80 inine methylation is important for efficient pRb C(term) phosphorylation, as manifested by the reduce

81 methylates pRb at the pRb C-terminal domain (pRb C(term)) on arginine (R) residues R775, R787, and R7

82 PRMT4 specifically methylates pRb at the pRb C-terminal domain (pRb C(term)) on arginine (R) resi

83 PRA cells Cx43 protein forms GJs, whereas in PRB cells the forward trafficking of Cx43 and GJ formati

84 hway restored the Cx43 trafficking defect in PRB cells.

85 cant downregulation of the tumor suppressors pRb, Cip/Kip cyclin-dependent kinase inhibitors (CKIs),

86 s reduction of 21% in the case that imported PRB coal replaces other coal sources in this Asian count

87 though the environmental impacts of shipping PRB coal to Asia are significant, the combination of sup

88 If instead PRB coal were to replace natural gas or nuclear generati

89 ship 8.8 million tons of Powder River Basin (PRB) coal annually to Asian markets via rail, river barg

90 While TAZ2 and pRb compete for binding to a monomeric E7 polypeptide, t

91 3F), disrupts the formation of the E2F-1/DP1-pRb complex in cells as well as in an isolated system.

92 s, and accordingly, a fraction of endogenous pRB constitutively associated with mitochondria.

93 which could help design better therapies for pRb-deficient cancer.

94 uggest that NANOS increases in importance in pRb-deficient cells and helps to maintain homeostasis by

95 However, in many contexts, the properties of pRb-deficient cells are similar to wild-type cells sugge

96 Overexpression of pRb delayed the viral protein production by wild-type MH

97 c repression at these elements that requires pRB-dependent recruitment of EZH2.

98 nistic studies revealed upregulation of p16, pRb dephosphorylation and its interaction with histone d

99 During osteoblast differentiation, pRB directly targets Alpl and Bglap, which encode the ma

100 t the heart of the pRB literature: What does pRB do?

101 Interestingly, the acute loss of pRb does not affect N-cadherin expression or migration o

102 lity in aquifer sediment (in particular, the PRB downstream linkage).

103 y regulates the tumor suppressor function of pRb during cell cycle control, in part by creating a bet

104 ecific genes are also cotargeted by E2F1 and pRB during differentiation along their respective lineag

105 repressor complex, is directly repressed by pRb/E2F in flies and humans.

106 lly related genes that are direct targets of pRb/E2F proteins.

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

108 , Rb(KO) caused similar increases in classic pRb/E2F-regulated transcripts in both tissues, but, unex

109 , decreasing the abundance of the inhibitory pRB-E2F1 complex and limiting G0/G1 arrest.

110 Thus, pRb-E2F1 is an obesity suppression mechanism in ARC POMC

111 senescence programs dampening the cyclin D1-pRb-E2F1 pathway.

112 l that TGFbeta induces autophagy through the pRb/E2F1 pathway and transcriptional activation of autop

113 rther highlight the central relevance of the pRb/E2F1 pathway downstream of TGFbeta signaling in tumo

114 ppressor protein/E2 promoter binding factor (pRb/E2F1) pathway, which we have previously established

115 We further determined that TGFbeta induces pRb/E2F1-dependent transcriptional activation of several

116 rate reduction for the same resources in the PRB: electrons and possibly reductase enzymes, and (4) c

117 r localization of Cx43 protein in PRA versus PRB expressing myocytes.

118 Loss of pRB-EZH2 complexes from repeats disperses H3K27me3 from

119 er, susceptibility to lymphoma suggests that pRB-EZH2 recruitment to repetitive elements may be cance

120 ion of E7 binding proteins beyond simply the pRb family members.

121 protein complexes, p300/CBP, TRRAP/p400, and pRb family members.

122 ese protein interactions, the interaction of pRb family proteins with conserved region 2 (CR2) of E1A

123 , through inactivating the activities of the pRb family proteins, is better understood than the activ

124 man papillomavirus type 16 E7, which targets pRb for degradation.

125 RB1 mutation, highlighting the importance of pRb for mitochondrial function and suggesting vulnerabil

126 teins, because E6 targets p53 and E7 targets pRb for rapid proteasome-mediated degradation.

127 that in vitro progesterone-liganded nuclear PRB forms a complex including JUN/JUN homodimers and P54

128 However, loss of pRb function does not fully account for potency of E7 in

129 Another mechanism of pRb function is repressing Skp2 to elevate p27 to arrest

130 ften caused by impairment of control through pRB function, but little is known about the interplay of

131 ceptor precursors in response to the loss of pRB function.

132 : (1) competition for H(2), (2) promotion of PRB growth due to having two electron acceptors (nitrate

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

134 lk with other proteins including p16(INK4A), pRB, HDM2 and p21(WAF1).

135 of the CDK activities that maintain p130 and pRB hyperphosphorylation for several hours after p107 de

136 Here, we report a nonnuclear role for pRB in apoptosis induction via pRB's direct participatio

137 iven the frequent functional inactivation of pRB in cancer, conditions that increase cohesion may pro

138 data establish a nontranscriptional role for pRB in direct activation of BAX and mitochondrial apopto

139 Despite evidence of a role for pRB in osteoblast differentiation, it is unknown whether

140 portantly, induced expression of mito-tagged pRB in Rb(-/-);p53(-/-) tumors was sufficient to block f

141 ners of B55alpha, which also associates with pRB in RCS cells.

142 Importantly, the regulatory functions of pRB in the cell cycle and differentiation are distinct b

143 cells resulted in an increased abundance of pRb in the cytoplasm, decreased overall levels of pRb, a

144 a critical Cdk phosphorylation motif, holds pRb in the hypophosphorylated growth-suppressing state.

145 cofactors that differentially interact with PRB in the presence of R5020 and MK+R5020.

146 K inhibits this mechanism by phosphorylating pRb in this location.

147 virus (MHV) A59 Nsp15 was also increased by pRb in vitro, and an MHV with mutations in the LXCXE/D-m

148 cumulation of perchlorate-reducing bacteria (PRB) in the biofilm are affected by four promotion or in

149 5) was stimulated by retinoblastoma protein (pRb) in vitro, and the two proteins can be coimmunopreci

150 ype and currently the circumstances in which pRB inactivation causes CIN in human cancers are unclear

151 the requirement of UL97 for these roles, as pRb inactivation induces CDK1, and CDK1 phosphorylates l

152 Our results demonstrate that pRb inactivation is insufficient to restore efficient vi

153 the transcriptional changes associated with pRb inactivation.

154 e advantage by virtue of its contribution to pRB inactivation.

155 e is associated with retinoblastoma protein (pRb) inactivation via sequential phosphorylation by the

156 on steps previously shown to be dependent on pRB, including recruitment of RNA polymerase II, are imp

157 On the other hand Cyclin D1 and pRb, indicating higher cell proliferation, were signific

158 Moreover, pRB interacted with BAX in vivo and could directly bind

159 demethylates histone H3 on Lys4 (H3K4), as a pRB-interacting protein counteracting pRB's role in prom

160 Our data revealed that E1A-CBP-pRb interactions have either positive or negative cooper

161 ut the allosteric effects at play in E1A-CBP-pRb interactions, or more generally in hub intrinsically

162 bility to dimerize, E7 recruits CBP/p300 and pRb into a ternary complex, bringing the histone acetylt

163 The retinoblastoma tumor suppressor protein pRb is a key regulator of cell cycle progression and med

164 Conversely, pRB is also recognized as an activator of tissue-specifi

165 The retinoblastoma tumor suppressor protein pRB is conventionally regarded as an inhibitor of the E2

166 y mitotic defects similar to those seen when pRB is depleted from non-transformed cells, but that the

167 Indeed, the interaction between BRG1 and pRB is enhanced during senescence.

168 pRb is frequently inactivated in tumours by mutations or

169 pRB is inactivated in many types of cancer and this rais

170 e previously showed that the inactivation of pRb is itself not sufficient to recapitulate the oncogen

171 anistically, promoter occupation by E2F1 and pRB is mutually dependent, and without this cooperative

172 One mechanism of tumour suppression by pRb is repressing E2F1.

173 tion of the retinoblastoma tumor suppressor (pRb) is a common oncogenic event that alters the express

174 how the structure of retinoblastoma protein (pRb) is altered by phosphorylation at T373 or S608.

175 The best-known target of RB protein (pRB) is the E2F transcription factor; however, many othe

176 es that occur when RBF1, the fly ortholog of pRB, is removed.

177 nes in Ishikawa cells stably expressing PRB (PRB-Ishikawa).

178 ccordingly, the acetylation-mimicking mutant PRB-K183Q exhibited accelerated DNA binding kinetics and

179 ental questions that sit at the heart of the pRB literature: What does pRB do?

180 pRB loss alters H4K20 methylation, a prerequisite for ef

181 ot a direct consequence of pRb loss; rather, pRb loss leads to the expansion and immortalization of a

182 show that defects in cohesion are key to the pRB loss phenotype.

183 precursor-specific circuitry cooperates with pRB loss to initiate this process and subsequently contr

184 at are transcriptionally down-regulated upon pRb loss, and we characterize two such candidates, MAP2K

185 ch could otherwise be induced in response to pRB loss.

186 hanges compromise mitotic fidelity following pRB loss.

187 these traits are not a direct consequence of pRb loss; rather, pRb loss leads to the expansion and im

188 The pRB-LxCxE interaction was not required for cell-cycle ar

189 Remarkably, the pRB-LxCxE interaction was not required for suppression o

190 Permeable reactive barriers (PRB) made of Fe(0) and in situ redox manipulation (ISRM)

191 this raises the possibility that the loss of pRB may be a general cause of CIN in tumors.

192 Of importance, PRA coexpression potentiated PRB-mediated migration, whereas PRA alone was ineffectiv

193 We investigated whether inactivation of pRb might overcome the requirement of UL97 for these rol

194 0 may compensate for loss of pRB, we studied pRB(N750F) activity in the presence and absence of p130.

195 Tumorspheres derived from pRb-negative tumors do not express pRb and express the n

196 zing datasets from normal retinal tissue and pRb-null retinoblastomas, we find a strong enrichment fo

197 Percutaneous renal biopsy (PRB) of kidney transplants might be prevented by an elev

198 greater activity compared with the wild-type PRB on genes containing progesterone response element.

199 the retinoblastoma tumor suppressor protein (pRb) on sites ordinarily phosphorylated by cyclin-depend

200 The Caenorhabditis elegans pRb ortholog, LIN-35, functions in a wide range of cellu

201 The retinoblastoma protein (pRb/p105) tumor suppressor plays a pivotal role in cell

202 The pocket proteins pRB, p107 and p130 have established roles in regulating

203 eficient in expression of 'pocket' proteins, pRb, p107 and p130, which are established targets of E7.

204 Mice null for pRb, p107, p130 or any combination of double mutants did

205 A (PP2A), and the large T antigen (LT) binds pRb, p107, p130, and p53.

206 pRb/p107-deficient mice developed head and neck cancer a

207 factor, which is negatively regulated by the pRB/p16(INK4a) tumor suppressor pathway, was implicated

208 Consistently, knockdown of pRB, p21(CIP1), and p16(INK4a), but not p53, suppressed

209 Studies revealed that tumor suppressors, pRb, p53, PTEN and Maf1 repress the transcription of Pol

210 This mechanism blocked pRb/p53 doubly deficient pituitary and prostate tumorige

211 essing SV40T, which functionally inactivates pRB/p53, markedly accelerated proliferation and cell-cyc

212 1/S molecules are the cell cycle inhibitors, pRb, p57, and variably, p21: none of the cyclins or cdks

213 c to epithelial cells, which is triggered by pRb pathway activation rather than p53 induction.

214 The p16(INK4a)-Cyclin D-CDK4/6-pRb pathway is dysregulated in 90% of melanomas.

215 he customary reference to the p16(INKA)/CDK4/pRB pathway may no longer be accurate; all PPs are poten

216 ion through canonical activation of the CDK4/pRB pathway.

217 The retinoblastoma protein (pRb) pathway represents a key component in the regulatio

218 n of 53BP1 in complex with a methylated K810 pRb peptide emphasized the role of the 53BP1 tandem tudo

219 pharmacological activation of AMPK, induces pRb phosphorylation and E2F target gene de-repression in

220 cell cycle, and we found that Pax6 inhibits pRb phosphorylation and represses genes involved in DNA

221 An increase in pRb phosphorylation has been previously linked to ischem

222 Early plus late cyclins and cdks, acting via pRb phosphorylation on distinct residues, complementaril

223 D1 (CCND1) and other G1-S cyclins, abolished pRb phosphorylation, and inhibited activation of S-phase

224 ow that shRNA targeting Cdc25A blocks Ser795 pRb phosphorylation.

225 repression inhibits retinoblastoma protein (pRb) phosphorylation, thereby limiting the transcription

226 in retinoblastoma tumor suppressor protein (pRb) phosphorylation.

227 ationship, they competed effectively with DB/PRB phylotypes such as Xanthomonadales and Rhodobacteral

228 Here, we investigated whether pRb plays a role in obesity.

229 We uncovered this activity by finding that pRB potentiated TNFalpha-induced apoptosis even when tra

230 Such an effect of PRB/PRA expression on FAK signaling might thus affect ad

231 et genes in Ishikawa cells stably expressing PRB (PRB-Ishikawa).

232 A methylmimetic form of pRb, pRb (R3F), disrupts the formation of the E2F-1/DP1-

233 These results suggest that the loss of pRB promotes segregation errors, whereas loss of p53 all

234 unit of a holoenzyme that phosphorylates the pRB protein and promotes G1/S cell-cycle progression and

235 nic fibroblasts and mice expressing a mutant pRB protein carrying an asparagine for phenylalanine sub

236 zyme that phosphorylates and inactivates the pRb protein.

237 The retinoblastoma tumor suppressor (pRb) protein associates with chromatin and regulates gen

238 ncluding Mip130, contains repressive E2F and pRB proteins.

239 iption factor E2F-1 and its interaction with pRb provide a key point of control in cell proliferation

240 using a Gal4-E2F-1 reporter system show that pRb (R3F) expression reduces the ability of pRb to repre

241 A methylmimetic form of pRb, pRb (R3F), disrupts the formation of the E2F-1/DP1-pRb c

242 ress E2F-1 transcriptional activation, while pRb (R3K) expression further represses E2F-1 transcripti

243 horylation of a methylation-impaired mutant, pRb (R3K).

244 pression increases following inactivation of pRb/RBF1 and becomes important for tissue homeostasis.

245 Its gene product (pRB) regulates transcription and is a negative regulator

246 DM5A and E2F4 gene targets were bound by the pRB-related protein p130, a DREAM complex component.

247 Indeed, in many regards, pRB remains an enigma.

248 Tumor suppressor pRb represses Skp2, a substrate-recruiting subunit of th

249 eview summarizes some recent developments in pRB research and focuses on progress toward answers for

250 ontributions of PR isoforms A and B (PRA and PRB, respectively) in cancer cell migration remains elus

251 mplicated in the activation of p107/p130 and pRB, respectively.

252 The retinoblastoma tumor suppressor protein pRb restricts cell growth through inhibition of cell cyc

253 This mito-tagged pRB retained the ability to promote apoptosis in respons

254 Its protein product, pRB (retinoblastoma protein), functions as a transcripti

255 ted a functional role for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in

256 ochondria, we generated a mutant that lacked pRB's classic nuclear roles.

257 lear role for pRB in apoptosis induction via pRB's direct participation in mitochondrial apoptosis.

258 se specific conformational changes and alter pRb's interaction with E2F via two distinct mechanisms.

259 To investigate the importance of pRB's LxCxE-interacting motif in cell-cycle control and

260 e well established, a precise description of pRB's mechanism of action has remained elusive.

261 , as a pRB-interacting protein counteracting pRB's role in promoting differentiation.

262 These results indicate that pRB's tumor suppressor activity is not effectuated by ac

263 of immunohistochemical expression of CDK4/6/pRb (S780).

264 These findings delineate a pRb-Skp2-p27-cyclin A-E2F1 pathway that determines wheth

265 Finally, by targeting pRB specifically to mitochondria, we generated a mutant

266 n- (Fe(0)) based permeable reactive barrier (PRB) systems for arsenic (As) remediation in the presenc

267 3-3sigma is required for the upregulation in PRB target gene expression following inhibition of Akt.

268 ent, is sufficient to upregulate a subset of PRB target genes in Ishikawa cells stably expressing PRB

269 ough gene ontology analysis of Akt-regulated PRB target genes, angiogenesis was found to be the princ

270 function and identifying binding partners of pRb, the challenge facing molecular biologists and clini

271 cells are synaptophysin-negative and express pRb, the epithelial cell marker cytokeratin that is expr

272 silicon and calcium coals, Utah Skyline and PRB, there was a secondary effect due to CO(2) and the h

273 Here we report a novel regulation of pRb through protein arginine methyltransferase 4 (PRMT4)

274 osphorylation of the retinoblastoma protein (pRb), thus blocking the activation of the myogenic switc

275 pRb (R3F) expression reduces the ability of pRb to repress E2F-1 transcriptional activation, while p

276 t kinases (CDK), inactivating the ability of pRb to repress host genes required for cell cycle progre

277 ion material in permeable reactive barriers (PRB) to treat Se-contaminated groundwater, and stable is

278 d response of the CDK4/6 target, phospho-Rb (pRb), to CDK4/6 inhibitors.

279 2alpha) and the retinoblastoma gene product, pRb, to regulate cell cycle exit.

280 st-translational modifications that occur on pRb together with its key effector E2F-1.

281 rrogate the mechanism by which Akt modulates PRB transcriptional activity, ChIP-Mass spectrometry was

282 h the p300 CH1 domain and the retinoblastoma pRb transcriptional repressor, whereas HPV16-E7 cannot.

283 aling downregulates progesterone receptor B (PRB) transcriptional activity, leading to overall impair

284 pRb tumor suppressor activity is governed by a variety o

285 ly unidentified role for 53BP1 in regulating pRb tumor suppressor activity.

286 eral studies have shown that the loss of the pRB tumor suppressor causes mitotic defects and chromoso

287 However, activation of either the p53 or pRB tumor suppressor pathway was sufficient to induce la

288 after Aurora B inhibition depends on p53 and pRB tumor suppressor pathways.

289 ted that loss of the retinoblastoma protein (pRB) tumor suppressor causes changes in centromere struc

290 cervical cancer, the p53 and retinoblastoma (pRb) tumor suppressor pathways are disrupted by the huma

291 These data explain how loss of pRB undermines genomic integrity.

292 moval, because of the beneficial effect from PRB using both acceptors.

293 nt evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-independent interaction with

294 Remarkably, we found that recombinant pRB was sufficient to trigger the BAX-dependent permeabi

295 reast cancer cell line expressing PRA and/or PRB, we analyzed the effect of conditional PR isoform ex

296 Because p130 may compensate for loss of pRB, we studied pRB(N750F) activity in the presence and

297 the retinoblastoma tumor suppressor protein (pRB), which is frequently inactivated in human cancer.

298 inhibitor BYL719 demonstrated suppression of pRB, while nonresponding tumors showed sustained or incr

299 omodimer interacts with the pocket domain of pRb, while the same region of the other E7 molecule bind

300 horylation and disrupting the interaction of pRb with E2F-1.