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1 all E2F family members tested (E2F1 through E2F5).
2 e 34 (Cdc34) and E2F transcription factor 5 (E2F5).
3 cyclin D1 and cdk4, pcna, cyclin G, Rb, and E2F5.
4 0 almost exclusively associate with E2F4 and E2F5.
5 TR sequences complementary to either E2F1 or E2F5.
6 ts by forming a ternary complex with E2f4 or E2f5 and Dp1 that binds and activates most of the genes
7 A crystal structure of the p107 CTD bound to E2F5 and its dimer partner DP1 reveals the molecular bas
8 o other kinases, transcription factors E2F4, E2F5, and p130, a DNA repair gene, a gene for the signal
12 affects the binding of E2F2, E2F3, E2F4, and E2F5 but significantly inhibits the binding of E2F1.
14 at LMP1 also blocks the function of E2F4 and E2F5 (E2F4/5) transcription factors through promoting th
17 her, this leads to the activation of E2F1 to E2F5, enhanced expression of E2F-responsive genes, and i
20 t that simultaneous inactivation of E2F4 and E2F5 in mice results in neonatal lethality, suggesting t
22 get genes related to cell mitosis and cycle, E2f5, Npm1, Cenpb, Rbbp6, and Scyl1, expressed in the he
28 a lesser extent E2F1, E2F3, and occasionally E2F5), was constitutively maintained at high levels inde
32 rminal activation domains of E2F1, E2F4, and E2F5, when fused to the Gal4 DNA binding domain, are suf
34 reporter assays and the transcription factor E2f5, which regulates CSF production, was verified as a
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