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1 h, we have unveiled a novel function for the transcription factor E2F.
2 binds and inactivates the pivotal cell-cycle transcription factor E2F.
3 ace through a pathway that is independent of transcription factor E2F.
4 P), but not by expression of subunits of the transcription factor E2F.
5 e kinase, and the large A/B pocket binds the transcription factor E2F.
6 ntering S phase is a rise in activity of the transcription factor E2F.
7 m of this site, there is a binding motif for transcription factor E2F.
8 omplexing with cellular proteins such as the transcription factor E2F.
9 ated with suppression of the activity of the transcription factor, E2F.
10 suppressors, pRb, p53, and p16INK4, and the transcription factor, E2F.
13 een the retinoblastoma protein (pRb) and the transcription factor E2F-1 are thought to be important f
14 ion analyses revealed that ASA inhibited the transcription factor E2F-1 binding activity to the survi
15 iously been shown that overexpression of the transcription factor E2F-1 can induce apoptosis in quies
17 y reported that forced overexpression of the transcription factor E2F-1 in human HT-1080 fibrosarcoma
18 binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the acti
22 nce of hypophosphorylated pRb and binding to transcription factor E2F-1 is consistent with ZD1694-ind
30 30 induction also decreased cyclin A and the transcription factor E2F-1 while increasing cyclin E at
33 e regulators: the Rb family of proteins, the transcription factor E2F-1, and the p21 family of protei
35 nant-negative mutants of the Rb gene, or the transcription factor E2F-1, which is a downstream target
36 prevented induction of the expression of the transcription factor E2F-1, which positively regulates t
42 Examination of the interactions involving transcription factor E2F activity during cell growth and
43 rate that PIN1 expression is mediated by the transcription factor E2F and enhanced by c-Neu and Ha-Ra
45 e cell cycle through its ability to bind the transcription factor E2F and repress transcription of ge
46 o target cancer cells with activation of the transcription factor E2F and the EGFR pathway by deletio
47 bly by promoting the DNA binding capacity of transcription factor E2F and thereby stabilizing the bas
50 ligodeoxynucleotides as "decoys" to trap the transcription factor E2F, and expression of a transgene
51 1a expression led to marked increases in the transcription factor E2F, and overexpression of E2F-1 al
53 artificial promoter carrying the cell cycle transcription factor E2F DNA-binding sequences and also
55 s gene repression mediated by the cell cycle transcription factor E2F (E2 promoter binding factor) an
56 stoma tumor suppressor protein (pRb) and the transcription factor E2F (E2F-1/ DP-1) in vitro and in v
58 e, promoter sequence analysis suggested that transcription factor E2F family is partially responsible
59 nes, but also, independent of the cell cycle transcription factor E2F, genes required for formative d
65 F-beta1 increased the binding of p107 to the transcription factor E2F, leading to decreased c-Myc pro
66 cognition sequences of the sequence-specific transcription factors E2F, NF-Y, AP-1, NF kappa B, and p
68 r protein Rb and alters its interaction with transcription factor E2F, presumably interfering with ce
71 nproliferating or growth-arrested cells, the transcription factor E2F remains bound to the retinoblas
73 product induces the binding of the cellular transcription factor E2F to the viral E2a promoter regio
74 with binding sites for the archetypal cancer transcription factor, E2F, were disproportionately overe
76 y through its action in binding the cellular transcription factor E2F, which activates genes importan
77 ls as a model to study the regulation of the transcription factor E2F, which is critically involved i
78 virus-mediated overexpression of the S phase transcription factor E2F, which is released after Rb pho