ライフサイエンスコーパス: Rb protein

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