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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
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
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.
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
39 t by binding and inducing the degradation of pRb and its related pocket protein family members, p107
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
47 correlate with the combined inactivation of pRB and p53 and that this association is evident in two
55 e cooperative effect of inactivation of both pRB and p53 tumor suppressor pathways that promotes CIN.
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
65 s, pyrosequencing illustrated that while DB, PRB, and SRB responded predictably to changes in accepto
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
73 to expression of a truncated LT that retains pRB binding but with a deletion of the C-terminal domain
78 Ewing sarcoma we report replacement of E2F3/pRB by constitutively expressed repressive E2F4/p130 com
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
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
89 ship 8.8 million tons of Powder River Basin (PRB) coal annually to Asian markets via rail, river barg
91 3F), disrupts the formation of the E2F-1/DP1-pRb complex in cells as well as in an isolated system.
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
98 nistic studies revealed upregulation of p16, pRb dephosphorylation and its interaction with histone d
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
108 , Rb(KO) caused similar increases in classic pRb/E2F-regulated transcripts in both tissues, but, unex
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
119 er, susceptibility to lymphoma suggests that pRB-EZH2 recruitment to repetitive elements may be cance
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
125 RB1 mutation, highlighting the importance of pRb for mitochondrial function and suggesting vulnerabil
127 that in vitro progesterone-liganded nuclear PRB forms a complex including JUN/JUN homodimers and P54
130 ften caused by impairment of control through pRB function, but little is known about the interplay of
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
135 of the CDK activities that maintain p130 and pRB hyperphosphorylation for several hours after p107 de
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
140 portantly, induced expression of mito-tagged pRB in Rb(-/-);p53(-/-) tumors was sufficient to block f
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.
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
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
159 demethylates histone H3 on Lys4 (H3K4), as a pRB-interacting protein counteracting pRB's role in prom
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
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
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
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.
178 ccordingly, the acetylation-mimicking mutant PRB-K183Q exhibited accelerated DNA binding kinetics and
181 ot a direct consequence of pRb loss; rather, pRb loss leads to the expansion and immortalization of a
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
187 these traits are not a direct consequence of pRb loss; rather, pRb loss leads to the expansion and im
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.
196 zing datasets from normal retinal tissue and pRb-null retinoblastomas, we find a strong enrichment fo
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
203 eficient in expression of 'pocket' proteins, pRb, p107 and p130, which are established targets of E7.
207 factor, which is negatively regulated by the pRB/p16(INK4a) tumor suppressor pathway, was implicated
209 Studies revealed that tumor suppressors, pRb, p53, PTEN and Maf1 repress the transcription of Pol
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
215 he customary reference to the p16(INKA)/CDK4/pRB pathway may no longer be accurate; all PPs are poten
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
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
225 repression inhibits retinoblastoma protein (pRb) phosphorylation, thereby limiting the transcription
227 ationship, they competed effectively with DB/PRB phylotypes such as Xanthomonadales and Rhodobacteral
229 We uncovered this activity by finding that pRB potentiated TNFalpha-induced apoptosis even when tra
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
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
242 ress E2F-1 transcriptional activation, while pRb (R3K) expression further represses E2F-1 transcripti
244 pression increases following inactivation of pRb/RBF1 and becomes important for tissue homeostasis.
246 DM5A and E2F4 gene targets were bound by the pRB-related protein p130, a DREAM complex component.
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
252 The retinoblastoma tumor suppressor protein pRb restricts cell growth through inhibition of cell cyc
255 ted a functional role for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in
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.
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
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
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
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
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
293 nt evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-independent interaction with
295 reast cancer cell line expressing PRA and/or PRB, we analyzed the effect of conditional PR isoform ex
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
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