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1 such as herpesvirus thymidine kinase and the retinoblastoma gene.
2  structural and functional features with the retinoblastoma gene and the retinoblastoma-related p107
3 ence similarity with pRB, the product of the retinoblastoma gene, and is a major E2F-associated prote
4 ts, exhibit bi-allelic mutations in RB1, the retinoblastoma gene, and lack of expression of the retin
5  known to inactivate pRB, the product of the retinoblastoma gene, and to enhance the action of p53.
6  lifespan and enable appropriate programs of retinoblastoma gene control during development.
7 nt mosaicism for the initial mutation in the retinoblastoma gene, either in the proband or in one of
8  binding to the products of the p300/CBP and retinoblastoma gene families.
9 cell cycle arrest mediated by members of the retinoblastoma gene family and can activate E2F1/DP1 and
10                                          The retinoblastoma gene family consisting of RB/p105, p107,
11 tumor-suppressor genes, or both, such as the retinoblastoma gene family members (RB/p105, p107, RB2/p
12          The single C. elegans member of the retinoblastoma gene family, lin-35 Rb, was originally id
13                  The proteins encoded by the retinoblastoma gene family, pRB, p107, and p130, have be
14 stoma; the initial oncogenic mutation in the retinoblastoma gene had been identified in these familie
15 GSEA analysis identified 'Adipogenesis' and 'retinoblastoma gene in cancer' as the top perturbed mole
16                   Targeted disruption of the retinoblastoma gene in mice leads to embryonic lethality
17 the HLH regulatory protein, Id2a, and of the retinoblastoma gene, p130, which regulates progression t
18 istinct from other mouse models in which the retinoblastoma gene pathway is disrupted and suggest tha
19             INK4a, a critical element of the retinoblastoma gene pathway, binds to and inhibits the a
20  a small interfering RNA (siRNA) against the retinoblastoma gene (pRb) and ectopic expression of huma
21 cdk9/cyclinT2 and the protein product of the retinoblastoma gene (pRb) in human cell lines.
22 hosphorylation of the protein product of the retinoblastoma gene, pRb.
23 mutant or null for p16 but wild-type for the retinoblastoma gene product (pRb) (MCF-7, MDA-MB-231, BT
24  papillomavirus type 16 (HPV16) binds to the retinoblastoma gene product (pRb) and dissociates pRb-E2
25 rly G1 phase prevents phosphorylation of the retinoblastoma gene product (pRb) and inhibits entry int
26 e cell cycle requires phosphorylation of the retinoblastoma gene product (pRb) by the cyclin D-depend
27 f E1A that inhibit the binding of E1A to the retinoblastoma gene product (pRb) further enhanced the s
28 en shown to phosphorylate histone H1 and the retinoblastoma gene product (pRb) in vitro.
29                                          The retinoblastoma gene product (pRb) interacts with many ce
30 man tumour cell lines that lack a functional retinoblastoma gene product (pRb) no cyclin D1-Cdk4 comp
31 dent kinase 4 (cdk4) complexes mediate early retinoblastoma gene product (pRb) phosphorylation in B-1
32                Among them are binding by the retinoblastoma gene product (pRb), activation by cdk3, a
33 ded that COL1A2 transactivation involves the retinoblastoma gene product (pRb), an activator of Sp1,
34 h as cyclins, cyclin-associated kinases, the retinoblastoma gene product (pRb), and E2F-1 function du
35 r alterations in expression of Ki-67, Bcl-2, retinoblastoma gene product (pRB), and p53 by immunohist
36  complex formation with proteins such as the retinoblastoma gene product (pRB), cyclin A and DP1.
37 transcription factors that interact with the retinoblastoma gene product (pRB), including members of
38 7 are nuclear phosphoproteins related to the retinoblastoma gene product (pRb).
39 cellular Unp specifically interacts with the retinoblastoma gene product (pRb).
40 to be responsible for phosphorylation of the retinoblastoma gene product (pRb).
41 its ability to be bound and regulated by the retinoblastoma gene product (pRb).
42 s), activity of cdks, and phosphorylation of retinoblastoma gene product (pRb).
43                         Co-expression of the retinoblastoma gene product (RB) abolishes baseline E2F-
44 as accompanied by hypophosphorylation of the retinoblastoma gene product (RB) and rapid down-regulati
45                                          The retinoblastoma gene product (Rb) is a tumor suppressor t
46 horbol 12-myristate 13-acetate (PMA) induced retinoblastoma gene product (Rb) phosphorylation, and ce
47                                          The retinoblastoma gene product (RB) regulates cell cycle, q
48                      Here we report that the retinoblastoma gene product (Rb) stimulates binding of t
49                                 However, the retinoblastoma gene product (RB), a cyclin-dependent kin
50                                              Retinoblastoma gene product (Rb), a negative regulator o
51 6-induced partial hypophosphorylation of the retinoblastoma gene product (Rb), observed in M1myc cell
52 d only as a consequence of the impairment in retinoblastoma gene product (Rb).
53 ssion, and led to hypophosphorylation of the retinoblastoma gene product (Rb).
54 ns, cyclin-dependent kinases (Cdks), and the retinoblastoma gene product (Rb).
55 to induce an enhanced phosphorylation of the retinoblastoma gene product and a synergistic increase i
56 K4 proteins block the phosphorylation of the retinoblastoma gene product and ARF protects p53 from de
57 Endostatin decreased the hyperphosphorylated retinoblastoma gene product and down-regulated cyclin D1
58  markers such as hyperphosphorylation of the retinoblastoma gene product and upregulation of the c-my
59 ively active nonphosphorylatable form of the retinoblastoma gene product blocked x-irradiation-induce
60 ombination of PA with okadaic acid prevented retinoblastoma gene product dephosphorylation induced by
61 t are mediated by PP1, such as apoptosis and retinoblastoma gene product dephosphorylation.
62                                          The retinoblastoma gene product has been implicated in the r
63 ited PDGF-induced SMC DNA synthesis by >95%, retinoblastoma gene product hyperphosphorylation by 90%,
64 with the ability of ceramide to activate the retinoblastoma gene product or to induce cell cycle arre
65 t did not change the cell cycle profile, nor retinoblastoma gene product phosphorylation state in DBD
66                                          The retinoblastoma gene product pRb and other members of the
67 pends on the interaction of large T with the retinoblastoma gene product pRb.
68 phase, E2F1/DP1 activity is repressed by the retinoblastoma gene product RB, which directly contacts
69  inhibitor as p130, a protein related to the retinoblastoma gene product Rb.
70 osed to CVT-313, hyperphosphorylation of the retinoblastoma gene product was inhibited, and progressi
71                                          The retinoblastoma gene product was localized to the nuclei
72 revented phosphorylation of CycD2-target Rb (retinoblastoma gene product) in vitro, and mice deficien
73 capacity to bind the cellular proteins p105 (retinoblastoma gene product), p107, and p300.
74               Altered phosphorylation of the retinoblastoma gene product, a critical cell cycle regul
75      In this setting, phosphorylation of the retinoblastoma gene product, a protein whose phosphoryla
76  S phase and prevents phosphorylation of the retinoblastoma gene product, DNA replication, clonal exp
77                                  Because the retinoblastoma gene product, pRB, is a known target for
78 ated polypeptide 2 alpha (Lap2alpha) and the retinoblastoma gene product, pRb, to regulate cell cycle
79  the phosphorylation and inactivation of the retinoblastoma gene product, pRB.
80                                          The retinoblastoma gene product, Rb, expressed in these cell
81                                          The retinoblastoma gene product, Rb, has previously been imp
82                              The role of the retinoblastoma gene product, RB, in transmitting the sig
83                                          The retinoblastoma gene product, Rb, is a cell cycle regulat
84                                          The retinoblastoma gene product, RB, seems to function as a
85 n the phosphorylation and degradation of the retinoblastoma gene product, Rb.
86                       On the other hand, the retinoblastoma gene product, which also regulates the G1
87 well as a decrease in phosphorylation of the retinoblastoma gene product.
88 ultimately affect the phosphorylation of the retinoblastoma gene product.
89 ssion of cyclin D and phosphorylation of the retinoblastoma gene product.
90 rrest and an increase in underphosphorylated retinoblastoma gene product.
91 s, stress-activated protein kinases, and the retinoblastoma gene product] that mediate its distinct c
92      Moreover, in vitro modifications of the retinoblastoma-gene-product-binding site of the c-fos pr
93 icate that the SV40T inactivation of p53 and retinoblastoma gene products, defects frequently found i
94 -specific control was provided by either the retinoblastoma gene promoter or the whey acidic protein
95                                          The retinoblastoma gene Rb is a prototype tumor suppressor w
96                                          The retinoblastoma gene Rb is the prototype tumor suppressor
97                          Inactivation of the retinoblastoma gene Rb leads to defects in cell prolifer
98                                          The retinoblastoma gene Rb was the first tumor suppressor ge
99 gion of chromosome 13q14.3, telomeric to the Retinoblastoma gene RB-1 is frequently deleted in patien
100               Mice with a single copy of the retinoblastoma gene (Rb(+/-)) develop a syndrome of mult
101 m embryos homozygous for a disruption of the retinoblastoma gene (Rb) exhibit a shorter G1 than their
102  of pRb in apoptosis, we examined endogenous retinoblastoma gene (Rb) expression following treatment
103  the physiological role of p107, a member of retinoblastoma gene (Rb) family, we disrupted the mouse
104                         Early studies of the retinoblastoma gene (RB) have uncovered its critical rol
105                        Overexpression of the retinoblastoma gene (Rb) in mice leads to the dwarf phen
106              Here we examine the role of the retinoblastoma gene (Rb) in myocyte survival.
107                                          The retinoblastoma gene (Rb) is mutated at significant frequ
108                                          The retinoblastoma gene (RB) is the prototypic tumor suppres
109                                          The retinoblastoma gene (Rb) regulates neural progenitor cel
110 l proliferation by BPV-1 E7 can occur in the retinoblastoma gene (Rb)-null cells, suggesting an Rb-in
111 scriptionally activated in cells lacking the retinoblastoma gene (Rb-/-).
112  mouse embryo fibroblasts (MEFs) lacking the retinoblastoma gene (Rb-1) have suggested that p130 and
113                                          The retinoblastoma gene (RB-1) was originally identified as
114   Although the involvement of p53 and of the retinoblastoma gene (RB/p105) in NPC has been well studi
115                                          The retinoblastoma gene, RB-1, was the first identified tumo
116                        Heterozygosity of the retinoblastoma gene Rb1 elicits tumorigenesis in suscept
117 homologous recombination (HR) deficiency and retinoblastoma gene (RB1) expression have been implicate
118                    Germline mutations of the retinoblastoma gene (RB1) predispose to both sporadic an
119                              Mutation of the retinoblastoma gene (RB1) tumour suppressor occurs in on
120 patient-derived xenograft models, as well as retinoblastoma gene (RB1)-deficient castration-resistant
121 r initiated by biallelic inactivation of the retinoblastoma gene (RB1).
122                                          The retinoblastoma gene, RB1, is frequently inactivated in a
123 amino acids and is the most divergent cloned retinoblastoma gene sequence to date.
124 mediated by transcriptional silencing of the retinoblastoma gene through epigenetic modifications med
125             Restoration of expression of the retinoblastoma gene to DU-145 prostate-cancer cells sens
126                 During this time period, the retinoblastoma gene was discovered; techniques for genet
127 eosarcomas often suffer mutations of the RB (retinoblastoma) gene, with resultant inactivation of the

 
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