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1 associates with an amino-terminal domain of Rb protein.
2 eration and this required its binding to the Rb protein.
3 n the nucleus where it co-localizes with the Rb protein.
4 itin require a physical interaction with the Rb protein.
5 tically active ROC1, and is protected by the Rb protein.
6 es Rb is by promoting the destabilization of Rb protein.
7 on in the E1A region responsible for binding Rb protein.
8 wth in the absence of detectable or inactive Rb protein.
9 deletion rendered Delta24 unable to bind the Rb protein.
10 vity of Cdk4 and Cdk6 and phosphorylation of Rb protein.
11 d cyclin E expression and hypophosphorylated Rb protein.
12 more of the putative cdk target sites of the RB protein.
13 , and the functional integrity of the entire RB protein.
14 s evidently more potent than the full-length RB protein.
15 ol III activity in the absence of functional Rb protein.
16 t result in absent or functionally defective Rb protein.
17 tumour was negative for p16 and positive for Rb protein.
18 3q14.2 loss (including RB1) and expressed no Rb protein.
19 might use a similar strategy to regulate the Rb protein.
20 icity of E1A for hypophosphorylated forms of RB proteins.
21 e levels of p67N-Myc and hyperphosphorylated Rb proteins.
22 requires its interactions with p300/CBP and RB proteins.
23 an LXCXE motif that directs association with Rb proteins.
24 proliferation requires T-antigen binding to Rb proteins.
25 gradation of p53 as well as interacting with Rb proteins.
26 ssors, including p53 and the retinoblastoma (RB) protein.
27 diated by phosphorylation of retinoblastoma (Rb) protein.
28 repressive functions of the retinoblastoma (Rb) protein.
29 negatively regulated by the retinoblastoma (RB) protein.
30 in, E7, that inactivates the retinoblastoma (Rb) protein.
31 in mammalian cells with the retinoblastoma (RB) protein.
32 minal 400 amino acids of the retinoblastoma (Rb) protein.
33 3, while E7 destabilizes the retinoblastoma (Rb) protein.
34 ation and loss of functional retinoblastoma (Rb) protein.
35 hat is also repressed by the Retinoblastoma (RB) protein.
36 duced phosphorylation of the retinoblastoma (Rb) protein.
37 escent tumor suppressor, the retinoblastoma (Rb) protein.
38 des a protein similar to the retinoblastoma (Rb) protein.
40 nteraction of TGase with the retinoblastoma (Rb) protein, a substrate of TGase that is also implicate
43 ignaling with a decreased phosphorylation of Rb protein and a low expression and binding of E2F1.
44 lating with decreased phosphorylation of the Rb protein and delayed cell proliferation in the hepFXR-
45 man ovarian cancer cell lines, we found that RB protein and mRNA were expressed at higher levels in c
47 of Ramos B cells leads to the degradation of Rb protein and phosphorylation of its family members, p1
48 zyme that phosphorylates and inactivates the Rb protein and promotes progression through G(1) to S ph
49 s coincided with the hyperphosphorylation of Rb protein and the early upregulation of cyclin D1 and c
50 as used to compare the overall expression of Rb protein and the kinetics of Rb hyperphosphorylation.
53 proteins associate with the cellular p53 and Rb proteins and interfere with their normal growth-regul
56 sted the requirement for the retinoblastoma (Rb) protein and its family members p107 and p130 in G0/G
58 ressor protein, binds to the retinoblastoma (Rb) protein and represses E2F transcriptional activity.
60 ty, dephosphorylation of the retinoblastoma (Rb) protein and the resultant G1 arrest of the cells.
62 As these cells exit the cell cycle, active Rb protein appears to exceed E2F, as there is a marked a
65 ose bladder cancer exhibit overexpression of RB protein as measured by immunohistochemical analysis d
68 lets, phosphorylation of the retinoblastoma (Rb) protein at both CDK2 and CDK4/6 sites was increased
71 oviral (E1A) deletion in the retinoblastoma (Rb) protein-binding region, substitution of the E1A prom
72 -2 cells lacking the p53 and retinoblastoma (Rb) proteins but that viral induction of fragility is re
73 ranscription in yeast cells and bind a plant Rb protein, but AtE2F2 cannot activate transcription or
75 lso confirmed through phosphorylation of the Rb protein by p15(INK4b) overexpression in the presence
76 hysical association between topo IIalpha and Rb protein by reciprocal immunoprecipitation and immunob
80 These results show that the inactivation of RB proteins causes metabolic reprogramming and that thes
81 e cell cycle dynamics of the retinoblastoma (RB) protein complex in the unicellular alga Chlamydomona
83 duction by IFN- gamma in the retinoblastoma (RB) protein-defective breast carcinoma line MDA-468-S4 (
84 ylation is well studied, proteasome-mediated RB protein degradation is emerging as an important regul
91 nduced, RB remained hyperphosphorylated, and RB protein expression and RB-E2F-1 association were mark
92 tion of Rb status, we observed a decrease in Rb protein expression in HTLV-1-infected cell lines as w
93 unohistochemistry demonstration of decreased RB protein expression in MCPyV-negative tumors and incre
97 pathological implications of retinoblastoma (RB) protein expression in these neoplasms, we examined t
98 nts of SVLT, which are unable to bind to the Rb protein family or induce neoplastic transformation, a
100 ized mice and nonhuman primates could detect RBD protein from transfected cells, as well as neutraliz
102 Recent discoveries of plant retinoblastoma (Rb) protein homologues and D-type cyclins suggest that c
104 , a phospho-specific Rb antibody showed much Rb protein in a hyperphosphorylated (inactive) form.
106 o E2F, likely due to the maintenance of most Rb protein in an inactive state by phosphorylation.
107 rovide evidence of an important role for the Rb protein in determining the degree of staurosporine-in
108 se analysis to show that the in vivo loss of Rb protein in E7-immortalized MECs is a consequence of e
109 These results indicate a key role for the Rb protein in the onset of neuron-neuroendocrine cell in
110 feration correlates with inactivation of the Rb protein in the T cell line Jurkat as well as human ao
112 Surprisingly, the steady-state level of Rb protein in these immortal cells was drastically decre
113 The expression of the exogenous wild-type RB protein in these tumor cell lines was driven by eithe
115 This review assesses the potential roles of Rb proteins in plant cell cycle control and development.
116 l proteins that modulate the retinoblastoma (Rb) protein in a manner classically defined as inactivat
118 igger phosphorylation of the retinoblastoma (Rb) protein in the mid- to late G1 phase of the cell cyc
124 teins, we show that unlike wild-type RB, PSM-RB proteins inhibit cell cycle progression in a broad ra
130 other substrates, such as the C terminus of Rb protein involved in c-Abl and histone deacetylase-1 (
134 fere with and/or control the function of the RB protein is critical for understanding both cell-cycle
135 ild type 3T3 L1 preadipocytes, we found that Rb protein is hyperphosphorylated early in adipogenesis,
144 , p53-independent apoptosis, retinoblastoma (RB) protein is hypophosphorylated to a p115 form by an a
145 nt cell cycle regulator, the retinoblastoma (Rb) protein, is often inactivated in many cancers includ
146 he LXCXE motif of T Ag binds directly to the RB proteins, it is not sufficient to fully inactivate th
147 cyclins, indicating that inhibition of their Rb protein kinase activities is due in part to the absen
149 um are characterized by hyper-phosphorylated RB protein, lack of G1 control, and rapid progression th
160 d proteases led to a marked stabilization of Rb protein, particularly the hypophosphorylated form.
163 creased cyclin D1 levels, CDK4 activity, and Rb protein phosphorylation were observed in 1-week ballo
164 ced cyclin D1 expression, CDK4 activity, and Rb protein phosphorylation, leading to VSMC growth and m
165 arked decrease in endogenous retinoblastoma (Rb) protein phosphorylation on cyclin D/CDK4-specific si
166 We further demonstrated that retinoblastoma (RB) protein plays a critical role in androgen regulation
170 45, which has a nonfunctional retinoblastoma Rb protein (pRb), were used to determine the possible me
172 ing the N-terminal truncated retinoblastoma (RB) protein (pRB94) completely suppressed the tumorigeni
176 In cells expressing a degradation-resistant RB protein (RB-MI), TNF-alpha does not activate c-ABL.
177 l 112 amino acid residues of the full-length RB protein (RB110), is a more potent tumor and growth su
178 rylation competent, amino-terminal-truncated Rb protein (Rb56) was a particularly potent inhibitor of
181 In mammalian cells, the retinoblastoma (RB) protein regulates G1 progression and functions throu
184 In cell culture systems, the inactivation of Rb proteins requires both a J domain in TAg that interac
185 Rb-binding motif and the "pocket domain" of Rb proteins responsible for Rb association with other ta
186 omains required for the interaction of R and Rb proteins reveals that R binds specifically to the N t
188 rrest at the R point with hypophosphorylated Rb protein, serum- or isoleucine-deprived cells experien
191 on from the rDNA reporter by retinoblastoma (Rb) protein, suggesting that the main mechanism by which
193 ycle-related upregulation of retinoblastoma (Rb) protein synthesis did not occur in the MV-Ed-infecte
194 nction of Egr-1 may involve the mediation of Rb protein that is essential to overcome the antiapoptot
197 mers form complexes with the retinoblastoma (Rb) protein, the Rb-related proteins p107 and p130, and
199 results suggest that the specific ability of Rb protein to interact with each E2F species, dependent
202 h lack BRG1 and also express a nonfunctional Rb protein, transcriptional repression by BRG1 was weak
203 and its cofactor DP1 increased, whereas the Rb protein underwent massive degradation without hyperph
205 or HPV-16 E7-induced enhanced degradation of Rb protein via a ubiquitin-proteasome pathway and sugges
206 e of the polypeptide chain derived for the C-Rb protein was confirmed using solution X-ray scattering
208 Rb-controlled pathways in the absence of the Rb protein was the reason for reduced viral productive r
210 ycle progression, the phosphorylation of the Rb protein, was altered in WM35N-ras; transforming growt
211 ty and turnover are controlled in this model RB protein, we assessed the impact of Cyclin-Cdk kinase
212 hyperphosphorylation of the retinoblastoma (Rb) protein, we examined the effects of salicylate on Rb
213 rylation competent and incompetent, of human Rb protein were evaluated for their ability to inhibit E
215 e full-length and the truncated forms of the RB protein, when overexpressed in tumor cells via replic
216 n reduced or deregulated levels of wild-type RB protein, whereas class 2 alleles result in mutant pro
217 erphosphorylated while cells in M0 contained Rb protein which was predominantly underphosphorylated.
218 roliferative activity, constitutively active RB proteins (which cannot be inactivated by phosphorylat
223 cycle block was reversed by inactivation of Rb proteins with viral oncoproteins such as polyoma larg
225 inactivation of the RB1 gene and the loss of Rb protein, yet the cell type in which Rb suppresses ret
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