ライフサイエンスコーパス: pRb

1 nic PFASs (AmPr-FHxSA, TAmPr-FHxSA, 6:2 FTSA-PrB).

2 a granular iron permeable reactive barrier (PRB).

3 inactivation of the retinoblastoma protein (pRb).

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

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

6 anism involving inactivation of both p53 and pRb.

7 that depends on the presence and nature of a PRB.

8 itrification, with and without a carbon-rich PRB.

9 activation of the tumor suppressors, such as pRb.

10 mors showed sustained or increased levels of pRB.

11 duced CIN in cancer cells lacking functional pRB.

12 E motif that is crucial for interaction with pRb.

13 nsformative pathways, including both p53 and pRb.

14 as well as the interaction between BRG1 and pRB.

15 selected patients with contraindications to PRB.

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

17 feasible and appears to be safe compared to PRB.

18 odeling factor that interacts with BRCA1 and pRB.

19 ruses that encode a protein to interact with pRb.

20 and inactivation of the cell cycle inhibitor pRb.

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

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

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

24 ithin and hydraulically down-gradient of the PRB.

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

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

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

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

29 Effects of pRB activation/inactivation on glutamine catabolism were

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

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

32 ess the E2F transcription factor family, but pRB also functions to regulate cellular differentiation

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

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

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

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

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

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

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

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

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

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

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

44 ubunit of the holoenzyme that phosphorylates pRB and NRF1 thereby governing cell-cycle progression an

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

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

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

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

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

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

51 When pRb and p53 are genetically inactivated, cells irreparab

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

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

54 pRb and p53 are the two major tumor suppressors.

55 pRb and p53 are two major tumor suppressors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 hway restored the Cx43 trafficking defect in PRB cells.

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

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

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

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

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

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

93 3F), disrupts the formation of the E2F-1/DP1-pRb complex in cells as well as in an isolated system.

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

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

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

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

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

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

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

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

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

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

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

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

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

107 analysis revealed a sustained disruption of pRB-E2F signaling by combination that was accompanied wi

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

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

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

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

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

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

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

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

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

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

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

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

120 ontaminant level (MCL) along segments of the PRB exhibiting upward trending influent TCE.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 We find that the presence of a carbon-rich PRB has a modest effect on the underlying soil microbial

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 pRb is frequently inactivated in tumours by mutations or

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

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

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

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

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

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

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

175 canonical function of the RB1 gene product, pRB, is to repress the E2F transcription factor family,

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

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

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

179 pRB loss alters H4K20 methylation, a prerequisite for ef

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

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

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

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

184 hanges compromise mitotic fidelity following pRB loss.

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

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

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

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

189 We find that the influence of both PRB materials is diminished at higher infiltration rates

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

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

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

193 0 may compensate for loss of pRB, we studied pRB(N750F) activity in the presence and absence of p130.

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

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

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

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

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

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

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

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

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

203 to the category regulated by pocket proteins pRb, p107, and p130.

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

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

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

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

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

211 1/S molecules are the cell cycle inhibitors, pRb, p57, and variably, p21: none of the cyclins or cdks

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

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

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

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

216 d by HPV oncoproteins, including the p53 and pRB pathways, or disrupt host defenses against viral inf

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

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

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

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

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

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

223 ow that shRNA targeting Cdc25A blocks Ser795 pRb phosphorylation.

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

225 in retinoblastoma tumor suppressor protein (pRb) phosphorylation.

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

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

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

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

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

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

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

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

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

235 zyme that phosphorylates and inactivates the pRb protein.

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

237 ncluding Mip130, contains repressive E2F and pRB proteins.

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

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

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

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

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

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

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

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

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

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

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

249 lar transcription factors, including p53 and pRb, respectively.

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

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

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

253 phase, such as cyclin-dependent kinases and pRb (retinoblastoma protein), are necessary for efficien

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

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

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

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

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

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

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

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

266 3-3sigma is required for the upregulation in PRB target gene expression following inhibition of Akt.

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

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

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

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

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

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

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

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

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

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

277 2alpha) and the retinoblastoma gene product, pRb, to regulate cell cycle exit.

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

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

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

281 pRb tumor suppressor activity is governed by a variety o

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

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

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

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

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

287 In the organic carbon PRB, unexpected negative europium anomalies were observe

288 ed that metastases preferentially inactivate pRB, upregulate the mTORC1 and WNT signaling pathways, a

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

290 s of methane within and down-gradient of the PRB varied widely from -94 per mille to -16 per mille; t

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

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

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

294 ations of trichloroethene (TCE) entering the PRB were as high as 10670 mug/L.

295 down-gradient of an organic carbon/limestone PRB were significantly reduced to <1% of influent levels

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

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

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

299 tin ligase, as an early repression target of pRb whose knockout blocked tumorigenesis in Rb1-deficien

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