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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.
39       Phosphorylation of the retinoblastoma (Rb) protein [a target of the cyclin D1/cyclin-dependent
40 nteraction of TGase with the retinoblastoma (Rb) protein, a substrate of TGase that is also implicate
41                                   Therefore, Rb proteins act as a central hub of quiescence and homeo
42 gested that tTG may modulate retinoblastoma (Rb) protein, an important suppressor of apoptosis.
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
46 l lines dramatically decreased expression of RB protein and mRNA.
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.
51               LeMSI1 also binds to the human RB protein and the RB-like RRB1 protein from maize, indi
52            T antigen interacts directly with Rb proteins and disrupts Rb-E2F complexes both in vitro
53 proteins associate with the cellular p53 and Rb proteins and interfere with their normal growth-regul
54       The recent discovery in plants of both Rb proteins and other components of the Rb pathway sugge
55 s in mammalian cells are the retinoblastoma (Rb) protein and close relatives.
56 sted the requirement for the retinoblastoma (Rb) protein and its family members p107 and p130 in G0/G
57 ower levels of Cyclin-D1 and retinoblastoma (Rb) protein and Rb phosphorylation.
58 ressor protein, binds to the retinoblastoma (Rb) protein and represses E2F transcriptional activity.
59 cts similar to the mammalian retinoblastoma (Rb) protein and the Rb-binding protein p48.
60 ty, dephosphorylation of the retinoblastoma (Rb) protein and the resultant G1 arrest of the cells.
61 ssociated factor), and H3K18ac; depletion of RB proteins; and transcriptional activation.
62   As these cells exit the cell cycle, active Rb protein appears to exceed E2F, as there is a marked a
63                                      Second, RB proteins are subject to proteasome-mediated destructi
64 well as the tumor suppressor retinoblastoma (Rb) protein are essential.
65 ose bladder cancer exhibit overexpression of RB protein as measured by immunohistochemical analysis d
66 etinoblastoma tumor suppressor gene protein (Rb protein) as substrate.
67                           Phosphorylation of Rb protein at both CDK2 and CDK4/CDK6 sites were signifi
68 lets, phosphorylation of the retinoblastoma (Rb) protein at both CDK2 and CDK4/6 sites was increased
69                                          The Rb protein became predominantly hypophosphorylated 48 h
70            After the loss of cell anchorage, Rb protein becomes hypophosphorylated in galectin-3-over
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
74                      Knockdown of endogenous RB protein by an Rb small inference RNA (siRNA) induced
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
77         However, striking differences in the Rb protein-caspase cleavage or hyperphosphorylation-in t
78 orhabditis elegans ortholog of the mammalian Rb protein, cause no obvious morphological defects.
79          Inactivation of the retinoblastoma (Rb) protein caused by gene mutation, association with on
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
82         Furthermore, a constitutively active RB protein could also inhibit the growth of RD cells wit
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
85                         The interaction with RB proteins displaces them from DNA-bound E2F transcript
86 rine development to regulate the activity of Rb proteins during cell division and proliferation.
87  proliferative state despite the presence of Rb proteins during development.
88 ation Id2 is a target of the retinoblastoma (Rb) protein during mouse embryogenesis.
89      Our data indicate that (i) E2F, DP, and Rb proteins each influence the selection of E2F-binding
90                          The retinoblastoma (Rb) protein exerts its tumor suppressor function primari
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
94                                   Absence of Rb protein expression indicative of pRb inactivation was
95                          Absent p16 and high RB protein expression was found in the tumors having los
96                              We investigated Rb protein expression, both total (phosphorylated and un
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
99 ology to the "pocket" A and B domains of the Rb protein family.
100 ized mice and nonhuman primates could detect RBD protein from transfected cells, as well as neutraliz
101                     Dephosphorylation of the RB protein has been reported to be associated with apopt
102  Recent discoveries of plant retinoblastoma (Rb) protein homologues and D-type cyclins suggest that c
103 vity was also elevated, concomitant with the RB protein hyperphosphorylation.
104 , a phospho-specific Rb antibody showed much Rb protein in a hyperphosphorylated (inactive) form.
105 sis revealed normal expression levels of the Rb protein in all carcinomas studied.
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
111 r IL-1 altered the phosphorylation status of RB protein in these cells.
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
114  the interaction between large T antigen and Rb proteins in JC virus-mediated oncogenesis.
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
117 hyperpohosphorylation of the Retinoblastoma (Rb) protein in PC-3 cells.
118 igger phosphorylation of the retinoblastoma (Rb) protein in the mid- to late G1 phase of the cell cyc
119 addition of soluble receptor-binding domain (RBD) proteins in the culture medium.
120                              Retinoblastoma (RB) protein inactivation during tumor progression is oft
121 of limb bud cells isolated from mice lacking Rb proteins individually or in combination.
122 sphorylation while reversing the decrease in Rb protein induced by DFMO.
123                             Changing the GST-RBD protein induction temperature from the original 37 t
124 teins, we show that unlike wild-type RB, PSM-RB proteins inhibit cell cycle progression in a broad ra
125                                              Rb protein inhibits both cell cycle progression and apop
126           Finally, physical association with Rb protein inhibits N5-induced apoptosis.
127                             Association with Rb protein inhibits p84N5-induced apoptosis suggesting t
128                              Retinoblastoma (Rb) proteins interact with E2F to regulate transcription
129                              In mammals, the Rb protein interacts specifically with D-type cyclins an
130  other substrates, such as the C terminus of Rb protein involved in c-Abl and histone deacetylase-1 (
131                                              Rb protein is a critical regulator of entry into the cel
132                                          The Rb protein is a tumor suppressor, which plays a pivotal
133                           The retinoblastoma Rb protein is an important factor controlling the cell c
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,
136                                   Therefore, Rb protein is not required for cell cycle control or dif
137 rest, indicating that interaction of LT with RB proteins is required to override p53 function.
138                          The retinoblastoma (RB) protein is a eukaryotic tumor suppressor and negativ
139                          The retinoblastoma (Rb) protein is a key cell-cycle regulator that controls
140                              Retinoblastoma (Rb) protein is a paradigm of tumor suppressors.
141                              Retinoblastoma (Rb) protein is a tumor suppressor that is dysregulated i
142 ation of the function of the retinoblastoma (Rb) protein is found in most human tumors.
143         The retinoblastoma tumor suppressor (RB) protein is functionally inactivated in the majority
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
148 The activation of Cdk4/6- and Cdk2-dependent Rb protein kinases is concomitantly blocked.
149 um are characterized by hyper-phosphorylated RB protein, lack of G1 control, and rapid progression th
150                                              Rb protein levels were 20-35-fold higher in primary huma
151 transfection assays indicated that decreased Rb protein levels were Tax dependent.
152 2 expression and a marked reduction in total Rb protein levels.
153 , a dominant effect of EBNA3C is to decrease Rb protein levels.
154 ad no effect on steady-state retinoblastoma (RB) protein levels or phosphorylation state.
155                          The retinoblastoma (Rb) protein negatively regulates the G1-S transition by
156                  A truncated retinoblastoma (RB) protein of approximately 94 kDa (RB94), lacking the
157 vel, p53 alteration, loss of retinoblastoma (Rb) protein or p16, and high bcl-2 level).
158 d binds host regulatory proteins such as the RB protein, p107, p130, and p300.
159 yclins D1, D2, D3, and E; p21; PCNA; and the Rb proteins, p107 and p130.
160 d proteases led to a marked stabilization of Rb protein, particularly the hypophosphorylated form.
161           MCM8 bound cyclin D1 and activated Rb protein phosphorylation by cyclin-dependent kinase 4
162  to account for inhibition of BCR-stimulated Rb protein phosphorylation by Fc gamma R.
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
167                                              Rb protein (pRb) expression was evaluated in 185 cases o
168                       It has been shown that Rb protein (pRb) is responsible for a major G1 checkpoin
169                     The best-known target of RB protein (pRB) is the E2F transcription factor; howeve
170 45, which has a nonfunctional retinoblastoma Rb protein (pRb), were used to determine the possible me
171                        There are three known Rb proteins, pRb, p130, and p107, all of which block the
172 ing the N-terminal truncated retinoblastoma (RB) protein (pRB94) completely suppressed the tumorigeni
173               Using recombinant E2F, DP, and Rb proteins prepared in baculovirus-infected cells and a
174                              Retinoblastoma (Rb) protein promotes cell survival after DNA damage.
175       We have designed constitutively active RB proteins, PSM-RB, that cannot be inactivated by phosp
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
179                                      E2F and RB proteins regulate the expression of genes involved in
180                          The retinoblastoma (RB) protein regulates cell proliferation and cell death.
181      In mammalian cells, the retinoblastoma (RB) protein regulates G1 progression and functions throu
182                                              Rb proteins represent an important target for viral onco
183                          The retinoblastoma (RB) protein represses global RNA polymerase III transcri
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
187    Further, p84N5 is a potential mediator of Rb protein's effects on DNA damage induced apoptosis.
188 rrest at the R point with hypophosphorylated Rb protein, serum- or isoleucine-deprived cells experien
189 ors capable of reversing the p27/myc/phospho-Rb protein signature.
190             Retinoblastoma tumor suppressor (Rb) protein stimulates macrophage differentiation by cou
191 on from the rDNA reporter by retinoblastoma (Rb) protein, suggesting that the main mechanism by which
192                                          The Rb protein suppresses development of an abnormal state o
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
195               Id2 is a natural target of the Rb protein that is recruited by Myc oncoproteins to bypa
196                                          The RBD proteins that rescue the infectivity of these defect
197 mers form complexes with the retinoblastoma (Rb) protein, the Rb-related proteins p107 and p130, and
198                              The addition of Rb protein to an in vitro gel shift binding assay stimul
199 results suggest that the specific ability of Rb protein to interact with each E2F species, dependent
200 alovirus (HCMV) requires the presence of the Rb protein to replicate efficiently.
201             ORC1 cooperates with SUV39H1 and RB protein to repress E2F1-dependent CCNE1 transcription
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
204                     Sequestration of p53 and Rb proteins using SV40 large T antigen completely rescue
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
207           No age-related difference in total Rb protein was observed in the Western blots; however, t
208 Rb-controlled pathways in the absence of the Rb protein was the reason for reduced viral productive r
209  co-localization of the endogenous BRCA1 and RB proteins was observed.
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
214              Moreover, the overall levels of Rb protein were significantly reduced within 6-12 hr of
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
219                                 We show that Rb proteins, which are major enforcers of quiescence, ma
220 is dependent on a functional retinoblastoma (RB) protein, which mediates downstream effects.
221 ed RB homologues, and results in a truncated RB protein with enhanced E2F binding affinity.
222 to phosphorylation to disrupt association of Rb proteins with appropriate binding targets.
223  cycle block was reversed by inactivation of Rb proteins with viral oncoproteins such as polyoma larg
224 of the HPV E7 gene causes down-regulation of Rb protein without inhibiting apoptosis.
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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