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1 ellular senescence through activation of the retinoblastoma tumor suppressor.
2 e regulator, was initially identified as the retinoblastoma tumor suppressor.
3 pocket family of proteins that includes the retinoblastoma tumor suppressor.
4 53 tumor suppressor, and the function of the retinoblastoma tumor suppressor.
5 (CDK2) and concomitant dephosphorylation of retinoblastoma tumor suppressor.
6 s deficient in MIF have significantly higher retinoblastoma tumor suppressor and lower E2F transcript
7 -phase entry through the inactivation of the retinoblastoma tumor suppressor and related pocket prote
8 e patterns--loss of H3K4 methylation--to the retinoblastoma tumor suppressor and the H3K4 demethylase
15 radiation (IR) and germline mutations in the retinoblastoma tumor suppressor gene (RB1) are the stron
22 ed from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not disp
23 dependent kinase activity phosphorylates Rb (retinoblastoma tumor suppressor gene product) family pro
24 lation of p27(kip1), hyperphosphorylation of retinoblastoma tumor suppressor gene product, and cellul
25 ro kinase assay using recombinant, truncated retinoblastoma tumor suppressor gene protein (Rb protein
35 wnregulate the levels of hyperphosphorylated retinoblastoma tumor-suppressor gene (Rb) and cyclin D1,
39 he function of short RNAs synergize with the retinoblastoma tumor suppressor homolog lin-35 in negati
41 16(INK4A) expression is not a consequence of retinoblastoma tumor suppressor inactivation but is trig
43 ggesting that in cervical cancer cells where retinoblastoma tumor suppressor is inactivated, CDK4/CDK
44 eins, which is essential for blockade of the retinoblastoma tumor suppressor, is also important for a
45 cyclin E promoter was repressed by wild-type Retinoblastoma tumor suppressor p105 protein (pRB) and b
46 action of E2F transcription factors and the retinoblastoma tumor suppressor/p107/p130 family of pock
48 whose inactivation suppresses defects in the retinoblastoma tumor suppressor pathway, and we successf
49 part independent of the inactivation of the retinoblastoma tumor suppressor pRb and is dependent on
53 cogenic activities is destabilization of the retinoblastoma tumor suppressor (pRB) through a ubiquiti
54 heterodimers from repression mediated by the retinoblastoma tumor suppressor (pRB) triggers cell cycl
55 E7 is its binding to and inactivation of the retinoblastoma tumor suppressor (pRb), but at least 18 o
56 to bind to and induce the degradation of the retinoblastoma tumor suppressor, pRb, and related "pocke
60 transcription factor E2F is a target of the retinoblastoma tumor suppressor protein (pRB) and may me
61 domain, which is required for binding of the retinoblastoma tumor suppressor protein (pRb) and pRb-li
62 of proliferation and differentiation by the retinoblastoma tumor suppressor protein (pRB) and relate
63 cells, CAK interacts with and phosphorylates retinoblastoma tumor suppressor protein (pRb) and retino
64 A oncoprotein can bind to and inactivate the retinoblastoma tumor suppressor protein (pRb) and the tr
65 ibits cell proliferation, interacts with the retinoblastoma tumor suppressor protein (pRb) and the tr
66 rgo G1 arrest because of inactivation of the retinoblastoma tumor suppressor protein (pRb) by the pap
67 suppressor protein or by inactivation of the retinoblastoma tumor suppressor protein (pRb) by transdu
69 studies have shown that inactivation of the retinoblastoma tumor suppressor protein (pRb) can cause
79 cells, p53, p21, Bax, and hypophosphorylated retinoblastoma tumor suppressor protein (pRb) levels inc
81 During infection, UL97 phosphorylates the retinoblastoma tumor suppressor protein (pRb) on sites o
82 Downregulation of Cdc25A led to reduction in retinoblastoma tumor suppressor protein (pRb) phosphoryl
84 cooperate with removal of the E2F inhibitor retinoblastoma tumor suppressor protein (pRB) to drive c
85 Only the under-phosphorylated form of the retinoblastoma tumor suppressor protein (pRB) was detect
86 le arrest depends on an interaction with the retinoblastoma tumor suppressor protein (pRb), but diffe
87 factors is the key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is
88 encode proteins that inactivate the cellular retinoblastoma tumor suppressor protein (pRb), which nor
89 nuclear p21, and hypophosphorylation of the retinoblastoma tumor suppressor protein (pRb), with no e
95 at least 3 h prior to phosphorylation of the retinoblastoma tumor suppressor protein (Rb) and the res
96 tumor-derived virus mutations do not affect retinoblastoma tumor suppressor protein (Rb) binding by
97 ment of E2F1 and concomitant dissociation of retinoblastoma tumor suppressor protein (Rb) from surviv
103 xhibit overexpression of hyperphosphorylated retinoblastoma tumor suppressor protein (Rb) or a marked
105 ibition of cyclin D3 and Cdk4 expression and retinoblastoma tumor suppressor protein (Rb) phosphoryla
109 fferentiation and hypophosphorylation of the retinoblastoma tumor suppressor protein (RB) typically a
110 Hepatitis C virus (HCV) downregulates the retinoblastoma tumor suppressor protein (Rb), a central
112 he pathway that controls the activity of the retinoblastoma tumor suppressor protein (Rb), which in t
122 e genes encoding TS and RR was enriched with retinoblastoma tumor suppressor protein and histone H3 t
124 cell cycle regulatory proteins including the retinoblastoma tumor suppressor protein and the coactiva
125 that was associated with phosphorylation of retinoblastoma tumor suppressor protein and the up-regul
127 of HPV-16 E7 involved in degradation of the retinoblastoma tumor suppressor protein as well as regio
128 phorylated growth inhibitory 105 kDa form of retinoblastoma tumor suppressor protein coimmunoprecipit
129 rmally RA-induced hypophosphorylation of the retinoblastoma tumor suppressor protein consistent with
130 not only by E2Fs but also by members of the retinoblastoma tumor suppressor protein family and by RN
131 Mutations which impaired binding of the retinoblastoma tumor suppressor protein family members p
135 n which we expressed a fragment of the human retinoblastoma tumor suppressor protein in fission yeast
136 iolet radiation-induced dephosphorylation of retinoblastoma tumor suppressor protein in human skin an
137 hosphorylation of this fragment of the human retinoblastoma tumor suppressor protein is dependent on
138 independent of its ability to inactivate the retinoblastoma tumor suppressor protein pRB and the rela
139 targets of the HPV-16 E7 oncoprotein are the retinoblastoma tumor suppressor protein pRB and the rela
140 teady-state level and metabolic half-life of retinoblastoma tumor suppressor protein pRB are decrease
145 osphorylated, growth suppressive form of the retinoblastoma tumor suppressor protein pRB was detected
146 ated family member, is in a complex with the retinoblastoma tumor suppressor protein Rb and activates
147 ntral ATPase domain, a domain that binds the retinoblastoma tumor suppressor protein Rb, and a C-term
148 cells, presumably because of mutation at the retinoblastoma tumor suppressor protein that allows func
149 M okadaic acid, resulted in an inhibition of retinoblastoma tumor suppressor protein translocation to
150 ted and ultraviolet-irradiated keratinocytes retinoblastoma tumor suppressor protein was localized to
151 tein, and accumulation of hypophosphorylated retinoblastoma tumor suppressor protein(105) was inhibit
153 functional role for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in dela
154 ts activation of p57Kip2 expression, and the retinoblastoma tumor suppressor protein, a known Id2 inh
155 pression of cyclin E, phosphorylation of the retinoblastoma tumor suppressor protein, and a doubling
156 ion-induced depletion in hyperphosphorylated retinoblastoma tumor suppressor protein, and accumulatio
157 in a rapid depletion in hyperphosphorylated retinoblastoma tumor suppressor protein, and the accumul
158 mmortalizing activity, LMP1 does not bind to retinoblastoma tumor suppressor protein, but instead blo
159 of transcription and differentiation by the retinoblastoma tumor suppressor protein, contains a JmjC
161 es 103 to 107), necessary for binding to the retinoblastoma tumor suppressor protein, pRB, and the re
162 E2F1 that facilitates complex formation with retinoblastoma tumor suppressor protein, pRB, and we fou
164 best known for its ability to inactivate the retinoblastoma tumor suppressor protein, pRb, many other
166 at examining the precise function(s) of the retinoblastoma tumor suppressor protein, RB, have been h
167 1/cip1) and promote dephosphorylation of the retinoblastoma tumor suppressor protein, Rb, in MCF-7 br
172 inetics, and relative phosphorylation of the retinoblastoma tumor suppressor protein, using primary t
183 nd maturation by TGFbeta is dependent on the retinoblastoma tumor suppressor protein/E2 promoter bind
196 In this regard, we have found that both the retinoblastoma tumor suppressor (Rb) and a novel nuclear
198 gh some E2F functions are independent of the Retinoblastoma tumor suppressor (Rb) and related family
201 y methylation were correlated with increased Retinoblastoma tumor suppressor (RB) expression, suggest
202 with earlier work, HPV16 E7 can bind to the retinoblastoma tumor suppressor (RB) family member p130
208 that only combined deletion of p27(Kip1) and retinoblastoma tumor suppressor (Rb) is sufficient to re
210 ) type 16 E7 oncoprotein must inactivate the retinoblastoma tumor suppressor (Rb) pathway to bypass G
224 1 is required for the destabilization of the retinoblastoma tumor suppressor RB1 in HPV16 E7-expressi
225 the cell cycle defects caused by loss of the retinoblastoma tumor suppressor-related protein encoded
226 UL97 phosphorylated and inactivated the retinoblastoma tumor suppressor, stimulated cell cycle p
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