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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.
7 nt mosaicism for the initial mutation in the retinoblastoma gene, either in the proband or in one of
9 cell cycle arrest mediated by members of the retinoblastoma gene family and can activate E2F1/DP1 and
11 tumor-suppressor genes, or both, such as the retinoblastoma gene family members (RB/p105, p107, RB2/p
14 stoma; the initial oncogenic mutation in the retinoblastoma gene had been identified in these familie
16 istinct from other mouse models in which the retinoblastoma gene pathway is disrupted and suggest tha
18 a small interfering RNA (siRNA) against the retinoblastoma gene (pRb) and ectopic expression of huma
21 mutant or null for p16 but wild-type for the retinoblastoma gene product (pRb) (MCF-7, MDA-MB-231, BT
22 papillomavirus type 16 (HPV16) binds to the retinoblastoma gene product (pRb) and dissociates pRb-E2
23 rly G1 phase prevents phosphorylation of the retinoblastoma gene product (pRb) and inhibits entry int
24 e cell cycle requires phosphorylation of the retinoblastoma gene product (pRb) by the cyclin D-depend
25 f E1A that inhibit the binding of E1A to the retinoblastoma gene product (pRb) further enhanced the s
28 man tumour cell lines that lack a functional retinoblastoma gene product (pRb) no cyclin D1-Cdk4 comp
29 dent kinase 4 (cdk4) complexes mediate early retinoblastoma gene product (pRb) phosphorylation in B-1
31 ded that COL1A2 transactivation involves the retinoblastoma gene product (pRb), an activator of Sp1,
32 h as cyclins, cyclin-associated kinases, the retinoblastoma gene product (pRb), and E2F-1 function du
33 r alterations in expression of Ki-67, Bcl-2, retinoblastoma gene product (pRB), and p53 by immunohist
35 transcription factors that interact with the retinoblastoma gene product (pRB), including members of
42 as accompanied by hypophosphorylation of the retinoblastoma gene product (RB) and rapid down-regulati
44 horbol 12-myristate 13-acetate (PMA) induced retinoblastoma gene product (Rb) phosphorylation, and ce
49 6-induced partial hypophosphorylation of the retinoblastoma gene product (Rb), observed in M1myc cell
53 to induce an enhanced phosphorylation of the retinoblastoma gene product and a synergistic increase i
54 K4 proteins block the phosphorylation of the retinoblastoma gene product and ARF protects p53 from de
55 Endostatin decreased the hyperphosphorylated retinoblastoma gene product and down-regulated cyclin D1
56 markers such as hyperphosphorylation of the retinoblastoma gene product and upregulation of the c-my
57 ively active nonphosphorylatable form of the retinoblastoma gene product blocked x-irradiation-induce
58 ombination of PA with okadaic acid prevented retinoblastoma gene product dephosphorylation induced by
61 ited PDGF-induced SMC DNA synthesis by >95%, retinoblastoma gene product hyperphosphorylation by 90%,
62 with the ability of ceramide to activate the retinoblastoma gene product or to induce cell cycle arre
63 t did not change the cell cycle profile, nor retinoblastoma gene product phosphorylation state in DBD
66 phase, E2F1/DP1 activity is repressed by the retinoblastoma gene product RB, which directly contacts
68 osed to CVT-313, hyperphosphorylation of the retinoblastoma gene product was inhibited, and progressi
70 revented phosphorylation of CycD2-target Rb (retinoblastoma gene product) in vitro, and mice deficien
74 S phase and prevents phosphorylation of the retinoblastoma gene product, DNA replication, clonal exp
76 ated polypeptide 2 alpha (Lap2alpha) and the retinoblastoma gene product, pRb, to regulate cell cycle
89 s, stress-activated protein kinases, and the retinoblastoma gene product] that mediate its distinct c
91 icate that the SV40T inactivation of p53 and retinoblastoma gene products, defects frequently found i
92 -specific control was provided by either the retinoblastoma gene promoter or the whey acidic protein
97 gion of chromosome 13q14.3, telomeric to the Retinoblastoma gene RB-1 is frequently deleted in patien
99 m embryos homozygous for a disruption of the retinoblastoma gene (Rb) exhibit a shorter G1 than their
100 of pRb in apoptosis, we examined endogenous retinoblastoma gene (Rb) expression following treatment
101 the physiological role of p107, a member of retinoblastoma gene (Rb) family, we disrupted the mouse
108 l proliferation by BPV-1 E7 can occur in the retinoblastoma gene (Rb)-null cells, suggesting an Rb-in
110 mouse embryo fibroblasts (MEFs) lacking the retinoblastoma gene (Rb-1) have suggested that p130 and
112 Although the involvement of p53 and of the retinoblastoma gene (RB/p105) in NPC has been well studi
120 mediated by transcriptional silencing of the retinoblastoma gene through epigenetic modifications med
123 eosarcomas often suffer mutations of the RB (retinoblastoma) gene, with resultant inactivation of the
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