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1 e regulator, was initially identified as the retinoblastoma tumor suppressor.
2  pocket family of proteins that includes the retinoblastoma tumor suppressor.
3 ellular senescence through activation of 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
9 ssing repressor or activator subunits of the retinoblastoma tumor suppressor complex (RBC).
10                           The product of the retinoblastoma tumor suppressor gene (Rb) can control ce
11                                          The retinoblastoma tumor suppressor gene (Rb) has many funct
12                              The loss of the retinoblastoma tumor suppressor gene (RB) is common in m
13 ctivity of a crucial E2F target in vivo, the retinoblastoma tumor suppressor gene (Rb).
14                                          The retinoblastoma tumor suppressor gene (RB-1) is a key reg
15                                          The retinoblastoma tumor suppressor gene (RB1) and its relat
16  by truncating mutations or deletions in the Retinoblastoma tumor suppressor gene (RB1) are frequentl
17 radiation (IR) and germline mutations in the retinoblastoma tumor suppressor gene (RB1) are the stron
18                                          The Retinoblastoma tumor suppressor gene (RB1) plays a role
19                                          The retinoblastoma tumor suppressor gene (RB1; encoding RB)
20                                          The retinoblastoma tumor suppressor gene plays important rol
21                                          The retinoblastoma tumor suppressor gene product (pRb) is in
22                                          The retinoblastoma tumor suppressor gene product (Rb) binds
23               Functional inactivation of the retinoblastoma tumor suppressor gene product (RB) is a c
24 ed from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not disp
25 dependent kinase activity phosphorylates Rb (retinoblastoma tumor suppressor gene product) family pro
26 lation of p27(kip1), hyperphosphorylation of retinoblastoma tumor suppressor gene product, and cellul
27 ro kinase assay using recombinant, truncated retinoblastoma tumor suppressor gene protein (Rb protein
28                             Mutations of the retinoblastoma tumor suppressor gene RB are frequently o
29                             Mutations in the retinoblastoma tumor suppressor gene Rb are involved in
30                                          The retinoblastoma tumor suppressor gene Rb is essential for
31 tremely sensitive to loss of function of the retinoblastoma tumor suppressor gene RB.
32 tic DNA templates and a PCR product from the retinoblastoma tumor suppressor gene.
33  DNA templates and on a PCR product from the retinoblastoma tumor suppressor gene.
34 d the inactivation of Rb, the product of the retinoblastoma tumor suppressor gene.
35 d in part by pRB, the protein product of the retinoblastoma tumor suppressor gene.
36                           The product of the retinoblastoma tumor-suppressor gene (pRB), a nuclear ph
37 wnregulate the levels of hyperphosphorylated retinoblastoma tumor-suppressor gene (Rb) and cyclin D1,
38                                          The retinoblastoma tumor-suppressor gene (Rb1) is centrally
39                                 Although the retinoblastoma tumor-suppressor gene (RB1) is frequently
40                             Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components
41 he function of short RNAs synergize with the retinoblastoma tumor suppressor homolog lin-35 in negati
42                                          The retinoblastoma tumor suppressor homolog MAT3 is a Volvox
43 16(INK4A) expression is not a consequence of retinoblastoma tumor suppressor inactivation but is trig
44                                          The retinoblastoma tumor suppressor is frequently inactivate
45 ggesting that in cervical cancer cells where retinoblastoma tumor suppressor is inactivated, CDK4/CDK
46 eins, which is essential for blockade of the retinoblastoma tumor suppressor, is also important for a
47 risk HPV E7 proteins to bind and degrade the retinoblastoma tumor suppressor or activate E2F target g
48 cyclin E promoter was repressed by wild-type Retinoblastoma tumor suppressor p105 protein (pRB) and b
49  action of E2F transcription factors and the retinoblastoma tumor suppressor/p107/p130 family of pock
50                      The p16(INK4a)-cyclin D-retinoblastoma tumor suppressor pathway is disrupted in
51 whose inactivation suppresses defects in the retinoblastoma tumor suppressor pathway, and we successf
52  part independent of the inactivation of the retinoblastoma tumor suppressor pRb and is dependent on
53                                          The retinoblastoma tumor suppressor pRB is required for skel
54                          Inactivation of the retinoblastoma tumor suppressor (pRB) alters the express
55                          Inactivation of the retinoblastoma tumor suppressor (pRb) is a common oncoge
56                                          The retinoblastoma tumor suppressor (pRb) protein associates
57 cogenic activities is destabilization of the retinoblastoma tumor suppressor (pRB) through a ubiquiti
58 heterodimers from repression mediated by the retinoblastoma tumor suppressor (pRB) triggers cell cycl
59 E7 is its binding to and inactivation of the retinoblastoma tumor suppressor (pRb), but at least 18 o
60 to bind to and induce the degradation of the retinoblastoma tumor suppressor, pRb, and related "pocke
61                                          The retinoblastoma tumor suppressor, pRB, plays a central ro
62 ion with p53, and partially resistant to the retinoblastoma tumor suppressor, pRB.
63           Mutations in the gene encoding the retinoblastoma tumor suppressor predispose humans and mi
64  transcription factor E2F is a target of the retinoblastoma tumor suppressor protein (pRB) and may me
65 domain, which is required for binding of the retinoblastoma tumor suppressor protein (pRb) and pRb-li
66  of proliferation and differentiation by the retinoblastoma tumor suppressor protein (pRB) and relate
67 cells, CAK interacts with and phosphorylates retinoblastoma tumor suppressor protein (pRb) and retino
68 A oncoprotein can bind to and inactivate the retinoblastoma tumor suppressor protein (pRb) and the tr
69 ibits cell proliferation, interacts with the retinoblastoma tumor suppressor protein (pRb) and the tr
70 rgo G1 arrest because of inactivation of the retinoblastoma tumor suppressor protein (pRb) by the pap
71 suppressor protein or by inactivation of the retinoblastoma tumor suppressor protein (pRb) by transdu
72                                          The retinoblastoma tumor suppressor protein (pRb) can associ
73  studies have shown that inactivation of the retinoblastoma tumor suppressor protein (pRb) can cause
74                                          The retinoblastoma tumor suppressor protein (pRB) can inhibi
75                          Inactivation of the retinoblastoma tumor suppressor protein (pRB) contribute
76                                          The retinoblastoma tumor suppressor protein (pRb) controls c
77       Viral oncoproteins that inactivate the retinoblastoma tumor suppressor protein (pRb) family bot
78           The E7 protein of HPV-16 binds all retinoblastoma tumor suppressor protein (pRB) family mem
79                          Inactivation of the retinoblastoma tumor suppressor protein (pRb) has been i
80                                              Retinoblastoma tumor suppressor protein (pRB) inhibition
81                                          The retinoblastoma tumor suppressor protein (pRB) is a trans
82                                          The retinoblastoma tumor suppressor protein (pRB) is a trans
83 cells, p53, p21, Bax, and hypophosphorylated retinoblastoma tumor suppressor protein (pRb) levels inc
84                                          The retinoblastoma tumor suppressor protein (pRB) negatively
85    During infection, UL97 phosphorylates the retinoblastoma tumor suppressor protein (pRb) on sites o
86 Downregulation of Cdc25A led to reduction in retinoblastoma tumor suppressor protein (pRb) phosphoryl
87                                The mammalian retinoblastoma tumor suppressor protein (pRb) regulates
88  cooperate with removal of the E2F inhibitor retinoblastoma tumor suppressor protein (pRB) to drive c
89    Only the under-phosphorylated form of the retinoblastoma tumor suppressor protein (pRB) was detect
90 le arrest depends on an interaction with the retinoblastoma tumor suppressor protein (pRb), but diffe
91  factors is the key downstream target of the retinoblastoma tumor suppressor protein (pRB), which is
92 encode proteins that inactivate the cellular retinoblastoma tumor suppressor protein (pRb), which nor
93  nuclear p21, and hypophosphorylation of the retinoblastoma tumor suppressor protein (pRb), with no e
94       The targets of E1A protein include the retinoblastoma tumor suppressor protein (pRb).
95 regulated most closely by phosphorylation of retinoblastoma tumor suppressor protein (pRb).
96 e of underphosphorylated, growth-suppressive retinoblastoma tumor suppressor protein (pRb).
97 of growth-regulatory proteins, including the retinoblastoma tumor suppressor protein (pRb).
98                            These include the retinoblastoma tumor suppressor protein (Rb) and histone
99 phate site to promote phosphorylation of the retinoblastoma tumor suppressor protein (Rb) and other s
100 at least 3 h prior to phosphorylation of the retinoblastoma tumor suppressor protein (Rb) and the res
101  tumor-derived virus mutations do not affect retinoblastoma tumor suppressor protein (Rb) binding by
102 ment of E2F1 and concomitant dissociation of retinoblastoma tumor suppressor protein (Rb) from surviv
103                         Disruption of murine retinoblastoma tumor suppressor protein (Rb) in mature p
104                                          The retinoblastoma tumor suppressor protein (RB) is a negati
105                                          The retinoblastoma tumor suppressor protein (RB) is a potent
106                            Expression of the retinoblastoma tumor suppressor protein (Rb) is required
107                                          The retinoblastoma tumor suppressor protein (RB) is targeted
108 xhibit overexpression of hyperphosphorylated retinoblastoma tumor suppressor protein (Rb) or a marked
109                                          The retinoblastoma tumor suppressor protein (Rb) pathway is
110 ibition of cyclin D3 and Cdk4 expression and retinoblastoma tumor suppressor protein (Rb) phosphoryla
111                                          The retinoblastoma tumor suppressor protein (RB) plays a cri
112                                          The retinoblastoma tumor suppressor protein (Rb) plays a vit
113                                          The retinoblastoma tumor suppressor protein (RB) plays an im
114                                          The retinoblastoma tumor suppressor protein (RB) plays impor
115 radigm for G1/S control, Cdks inactivate the retinoblastoma tumor suppressor protein (Rb) through pho
116 fferentiation and hypophosphorylation of the retinoblastoma tumor suppressor protein (RB) typically a
117    Hepatitis C virus (HCV) downregulates the retinoblastoma tumor suppressor protein (Rb), a central
118                                          The retinoblastoma tumor suppressor protein (RB), a critical
119 he pathway that controls the activity of the retinoblastoma tumor suppressor protein (Rb), which in t
120 t inducible in tumor cells defective for the retinoblastoma tumor suppressor protein (Rb).
121 ent kinase activity, and underphosphorylated retinoblastoma tumor suppressor protein (RB).
122 h encodes proteins capable of binding to the retinoblastoma tumor suppressor protein (Rb).
123 ells, a key regulator of this process is the retinoblastoma tumor suppressor protein (RB).
124  the hypophosphorylated (active) form of the retinoblastoma tumor suppressor protein (Rb).
125 7 is associated with its ability to bind the retinoblastoma tumor suppressor protein (Rb).
126 e to bind to and inhibit the function of the retinoblastoma tumor suppressor protein (RB).
127 on-gamma, in solid tumor cells, requires the retinoblastoma tumor suppressor protein (Rb).
128             Interestingly, cells lacking the retinoblastoma tumor suppressor protein also display arr
129 e genes encoding TS and RR was enriched with retinoblastoma tumor suppressor protein and histone H3 t
130                                          The retinoblastoma tumor suppressor protein and its family m
131 cell cycle regulatory proteins including the retinoblastoma tumor suppressor protein and the coactiva
132  that was associated with phosphorylation of retinoblastoma tumor suppressor protein and the up-regul
133                 Western blot analysis of the retinoblastoma tumor suppressor protein antigen from ker
134  of HPV-16 E7 involved in degradation of the retinoblastoma tumor suppressor protein as well as regio
135 phorylated growth inhibitory 105 kDa form of retinoblastoma tumor suppressor protein coimmunoprecipit
136 rmally RA-induced hypophosphorylation of the retinoblastoma tumor suppressor protein consistent with
137  not only by E2Fs but also by members of the retinoblastoma tumor suppressor protein family and by RN
138      Mutations which impaired binding of the retinoblastoma tumor suppressor protein family members p
139                                          The retinoblastoma tumor suppressor protein has been shown t
140                                          The retinoblastoma tumor suppressor protein has been shown t
141                Both protein kinase C and the retinoblastoma tumor suppressor protein have been linked
142 n which we expressed a fragment of the human retinoblastoma tumor suppressor protein in fission yeast
143 iolet radiation-induced dephosphorylation of retinoblastoma tumor suppressor protein in human skin an
144 hosphorylation of this fragment of the human retinoblastoma tumor suppressor protein is dependent on
145 independent of its ability to inactivate the retinoblastoma tumor suppressor protein pRB and the rela
146 targets of the HPV-16 E7 oncoprotein are the retinoblastoma tumor suppressor protein pRB and the rela
147 teady-state level and metabolic half-life of retinoblastoma tumor suppressor protein pRB are decrease
148                                      E2F and retinoblastoma tumor suppressor protein pRB are importan
149                                          The retinoblastoma tumor suppressor protein pRb is a key reg
150                                          The retinoblastoma tumor suppressor protein pRB is conventio
151                                          The retinoblastoma tumor suppressor protein pRb restricts ce
152 osphorylated, growth suppressive form of the retinoblastoma tumor suppressor protein pRB was detected
153 ated family member, is in a complex with the retinoblastoma tumor suppressor protein Rb and activates
154 ntral ATPase domain, a domain that binds the retinoblastoma tumor suppressor protein Rb, and a C-term
155 cells, presumably because of mutation at the retinoblastoma tumor suppressor protein that allows func
156 M okadaic acid, resulted in an inhibition of retinoblastoma tumor suppressor protein translocation to
157 ted and ultraviolet-irradiated keratinocytes retinoblastoma tumor suppressor protein was localized to
158 tein, and accumulation of hypophosphorylated retinoblastoma tumor suppressor protein(105) was inhibit
159 tion of growth inhibitory hypophosphorylated retinoblastoma tumor suppressor protein(105).
160  functional role for the cyclin D1/Cdk4/pRb (retinoblastoma tumor suppressor protein) pathway in dela
161 ts activation of p57Kip2 expression, and the retinoblastoma tumor suppressor protein, a known Id2 inh
162 pression of cyclin E, phosphorylation of the retinoblastoma tumor suppressor protein, and a doubling
163 ion-induced depletion in hyperphosphorylated retinoblastoma tumor suppressor protein, and accumulatio
164  in a rapid depletion in hyperphosphorylated retinoblastoma tumor suppressor protein, and the accumul
165 mmortalizing activity, LMP1 does not bind to retinoblastoma tumor suppressor protein, but instead blo
166  of transcription and differentiation by the retinoblastoma tumor suppressor protein, contains a JmjC
167                        Interestingly, unlike retinoblastoma tumor suppressor protein, MDMX, and p14(A
168 es 103 to 107), necessary for binding to the retinoblastoma tumor suppressor protein, pRB, and the re
169 E2F1 that facilitates complex formation with retinoblastoma tumor suppressor protein, pRB, and we fou
170              In vitro phosphorylation of the retinoblastoma tumor suppressor protein, pRB, by cyclin
171 best known for its ability to inactivate the retinoblastoma tumor suppressor protein, pRb, many other
172                                          The retinoblastoma tumor suppressor protein, RB, contains at
173  at examining the precise function(s) of the retinoblastoma tumor suppressor protein, RB, have been h
174 1/cip1) and promote dephosphorylation of the retinoblastoma tumor suppressor protein, Rb, in MCF-7 br
175                                          The retinoblastoma tumor suppressor protein, Rb, interacts d
176                                          The retinoblastoma tumor suppressor protein, RB, is a negati
177          The antiproliferative action of the retinoblastoma tumor suppressor protein, RB, is disrupte
178 cogene that functions by inactivation of the retinoblastoma tumor suppressor protein, RB.
179 inetics, and relative phosphorylation of the retinoblastoma tumor suppressor protein, using primary t
180 d overriding the checkpoint functions of the retinoblastoma tumor suppressor protein.
181 and depletion of hyperphosphorylation of the retinoblastoma tumor suppressor protein.
182 sphorylated and hyperphosphorylated forms of retinoblastoma tumor suppressor protein.
183 accompanied by unchecked inactivation of the retinoblastoma tumor suppressor protein.
184 k4/6 activity and active, hypophosphorylated retinoblastoma tumor suppressor protein.
185  generation of a complex also containing the retinoblastoma tumor suppressor protein.
186 ed because its gene products can bind to the retinoblastoma tumor suppressor protein.
187 ependent of the ability of E7 to inhibit the retinoblastoma tumor suppressor protein.
188 lix-loop-helix transcription factors and the retinoblastoma tumor suppressor protein.
189 ays and inhibition of phosphorylation of the retinoblastoma tumor suppressor protein.
190 nd maturation by TGFbeta is dependent on the retinoblastoma tumor suppressor protein/E2 promoter bind
191                                          The retinoblastoma tumor-suppressor protein (pRb) is a criti
192                                          The retinoblastoma tumor-suppressor protein (pRb) is known t
193                                          The retinoblastoma tumor-suppressor protein (RB) is an impor
194                                          The retinoblastoma tumor-suppressor protein (Rb) plays a cri
195                                          The retinoblastoma tumor-suppressor protein, pRb, is a membe
196 receptor that is negatively regulated by the retinoblastoma tumor-suppressor protein.
197 F-1/DP1 transcription factor complex and the retinoblastoma tumor-suppressor protein.
198 g their cellular targets are the p53 and the retinoblastoma tumor suppressor proteins.
199                                          The retinoblastoma tumor suppressor RB and its related prote
200                                          The retinoblastoma tumor suppressor RB controls the prolifer
201                         In cancer cells, the retinoblastoma tumor suppressor RB is directly inactivat
202                                          The retinoblastoma tumor suppressor RB is the downstream med
203                                          The retinoblastoma tumor suppressor RB is well known for its
204  In this regard, we have found that both the retinoblastoma tumor suppressor (Rb) and a novel nuclear
205                                          The retinoblastoma tumor suppressor (RB) and mismatch repair
206 gh some E2F functions are independent of the Retinoblastoma tumor suppressor (Rb) and related family
207                           E-cadherin and the retinoblastoma tumor suppressor (Rb) are traditionally a
208                                          The retinoblastoma tumor suppressor (Rb) controls the prolif
209 y methylation were correlated with increased Retinoblastoma tumor suppressor (RB) expression, suggest
210  with earlier work, HPV16 E7 can bind to the retinoblastoma tumor suppressor (RB) family member p130
211                                          The retinoblastoma tumor suppressor (RB) is a central cell c
212                                          The retinoblastoma tumor suppressor (RB) is a critical regul
213                                          The retinoblastoma tumor suppressor (Rb) is a multifunctiona
214                                          The retinoblastoma tumor suppressor (RB) is crucial for the
215                                          The retinoblastoma tumor suppressor (RB) is functionally ina
216                                          The retinoblastoma tumor suppressor (RB) is functionally ina
217                                          The retinoblastoma tumor suppressor (RB) is functionally ina
218 that only combined deletion of p27(Kip1) and retinoblastoma tumor suppressor (Rb) is sufficient to re
219                         The integrity of the retinoblastoma tumor suppressor (RB) pathway is critical
220 ) type 16 E7 oncoprotein must inactivate the retinoblastoma tumor suppressor (Rb) pathway to bypass G
221                              The role of the retinoblastoma tumor suppressor (RB) pathway, which is l
222  we demonstrate that Plk1 is a target of the retinoblastoma tumor suppressor (RB) pathway.
223 n is common in DCIS, as is disruption of the retinoblastoma tumor suppressor (RB) pathway.
224 oncogenic pathway and/or inactivation of the retinoblastoma tumor suppressor (RB) pathway.
225                                          The retinoblastoma tumor suppressor (RB) plays an important
226 eraction between CHT7 and the C. reinhardtii retinoblastoma tumor suppressor (RB) protein homolog MAT
227                                          The retinoblastoma tumor suppressor (RB) protein is function
228                                              Retinoblastoma tumor suppressor (Rb) protein stimulates
229 and has been implicated in the action of the retinoblastoma tumor suppressor (RB).
230 eminin is regulated transcriptionally by the retinoblastoma tumor suppressor (RB)/E2F pathway.
231                                          The retinoblastoma tumor suppressor, RB, assembles multiprot
232                                          The retinoblastoma tumor suppressor, RB, is a key regulator
233                                          The retinoblastoma tumor suppressor, RB, is a negative regul
234                                          The retinoblastoma tumor suppressor, RB, is thought to inhib
235 1 is required for the destabilization of the retinoblastoma tumor suppressor RB1 in HPV16 E7-expressi
236 sing an HPV16 E7 variant that can inactivate retinoblastoma tumor suppressor (RB1) but cannot degrade
237 the cell cycle defects caused by loss of the retinoblastoma tumor suppressor-related protein encoded
238 cus 3-4 (mat3-4), which contains a defective retinoblastoma tumor suppressor-related protein of Chlam
239      UL97 phosphorylated and inactivated the retinoblastoma tumor suppressor, stimulated cell cycle p
240  and cyclin A-dependent phosphorylation of a retinoblastoma tumor suppressor substrate.

 
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