ライフサイエンスコーパス: E2F5

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 pment, but little is known about the role of E2F5.

6 TR sequences complementary to either E2F1 or E2F5.

7 ts by forming a ternary complex with E2f4 or E2f5 and Dp1 that binds and activates most of the genes

8 A crystal structure of the p107 CTD bound to E2F5 and its dimer partner DP1 reveals the molecular bas

9 o other kinases, transcription factors E2F4, E2F5, and p130, a DNA repair gene, a gene for the signal

10 Thus, E2F4 and E2F5 are dispensable for cell cycle progression but nece

11 e growth factor (NGF), while E2F1, E2F3, and E2F5 are downregulated.

12 miRNA target databases predicted E2F1 and E2F5 as putative targets.

13 affects the binding of E2F2, E2F3, E2F4, and E2F5 but significantly inhibits the binding of E2F1.

14 of negative cell cycle regulators including E2f5, Cdkn1c, Ccne1 and Wee1.

15 larities to MMTV-Neu tumors, suggesting that E2F5 conditional knockout mammary glands and tumors may

16 However, after a prolonged latency the E2F5 conditional knockout mice developed highly metastat

17 E2F4 and E2F5 constitute a defined subset of the family.

18 that the E2F transcription factors E2F4 and E2F5 directly regulate NIK transcription and are require

19 at LMP1 also blocks the function of E2F4 and E2F5 (E2F4/5) transcription factors through promoting th

20 E2F2, and E2F3a) or repressors (E2F3b, E2F4, E2F5, E2F6, and E2F7).

21 Interaction between NS1 and E2F4 or E2F5 enhanced the nuclear import of these repressive E2F

22 her, this leads to the activation of E2F1 to E2F5, enhanced expression of E2F-responsive genes, and i

23 y viral factor responsible for altering E2F1-E2F5 expression, but not E2F6-E2F8 expression.

24 ts the control of expression of the E2F4 and E2F5 genes.

25 t that simultaneous inactivation of E2F4 and E2F5 in mice results in neonatal lethality, suggesting t

26 signature tools demonstrated the presence of E2F5 in the mammary gland and showed changes in predicte

27 study demonstrates that conditional loss of E2F5 in the mammary gland leads to tumor formation, reve

28 ry function, we generated a mammary-specific E2F5 knockout mouse model, resulting in modest mammary g

29 d on these findings, we propose that loss of E2F5 leads to altered regulation of Cyclin D1, which fac

30 repressing a network of oncogenes including E2F5, LIN28B, MYC and NRAS.

31 get genes related to cell mitosis and cycle, E2f5, Npm1, Cenpb, Rbbp6, and Scyl1, expressed in the he

32 ng to p130 but had no effect on E2F4/p107 or E2F5/p130 complexes.

33 shift with the antibody against the E2F4 and E2F5 pocket protein, p107.

34 f miR-205 in melanoma cells reduced E2F1 and E2F5 protein levels.

35 But, unlike the E2F4 and E2F5 proteins, which are also expressed in quiescent cel

36 Testing the hypothesis that E2F5 regulates mammary function, we generated a mammary-

37 Downstream E2F4/E2F5 targets, which are potentially involved in the prog

38 a lesser extent E2F1, E2F3, and occasionally E2F5), was constitutively maintained at high levels inde

39 The expression levels of E2F1 and E2F5 were correlated inversely with that of miR-205 in m

40 Accordingly, E2F1 to E2F3 but not E2F4 and E2F5 were found to bind sp1 in vitro.

41 sent in E2F2 and E2F3 but absent in E2F4 and E2F5, were essential.

42 rminal activation domains of E2F1, E2F4, and E2F5, when fused to the Gal4 DNA binding domain, are suf

43 In humans, Rb binds E2F1-E2F5, whereas p107 and p130 almost exclusively associate

44 ally with the cell-cycle regulators E2F4 and E2F5, which enables them to activate distinct sets of ta

45 reporter assays and the transcription factor E2f5, which regulates CSF production, was verified as a