ライフサイエンスコーパス: E2F7

1 or repressors (E2F3b, E2F4, E2F5, E2F6, and E2F7).

2 anism for the repression of transcription by E2F7.

3 3 being sufficient to increase expression of E2F7.

4 a novel E2F family member, which we now term E2F7.

5 tocol revealed that combined inactivation of E2f7/8 enhanced tumorigenesis and accelerated malignant

6 Caenorhabditis elegans, we identify a novel E2F7/8 homolog, EFL-3, and show that EFL-3 functions coo

7 ndicating that the tumor-promoting effect of E2F7/8 inactivation can be partially compensated via E2F

8 -deficient neoplastic cells, indicating that E2F7/8 might inhibit intratumoral vessel branching via i

9 chanism of the tumor suppressor functions of E2F7/8 remain obscure.

10 Importantly, E2F7/8 repressed a large set of E2F target genes that ar

11 We show that loss of E2F7/8 triggers apoptosis via induction of E2F1 in respo

12 hanced intratumoral branching in xenografted E2f7/8-deficient neoplasms compared with E2f7/8-proficie

13 itor of vascular branching, was decreased in E2f7/8-deficient neoplastic cells, indicating that E2F7/

14 or successful isolation and establishment of E2f7/8-deficient primary keratinocyte cultures was much

15 Moreover, E2f7/8-deficient primary keratinocytes proliferate more

16 ted E2f7/8-deficient neoplasms compared with E2f7/8-proficient neoplasms.

17 risingly, concomitant inactivation of Rb and E2f7, a close family member of E2f8, did not substantial

18 These results identify E2F7 and E2F8 as a unique repressive arm of the E2F tran

19 se observations, together with the fact that E2F7 and E2F8 can homodimerize and are expressed in the

20 The E2f7 and E2f8 family members are thought to function as

21 the function of the atypical repressor genes E2f7 and E2f8 in adult liver physiology.

22 ice, we determined that combined deletion of E2f7 and E2f8 in hepatocytes leads to HCC.

23 ve analyzed the consequences of inactivating E2f7 and E2f8 in mice and show that their individual los

24 prisingly, keratinocyte-specific deletion of E2F7 and E2F8 in mice did not interfere with skin develo

25 nce-mediated (CRISPRi-mediated) silencing of E2F7 and E2F8 in miR-142-deficient T cells ameliorated c

26 ctors consisting of the two atypical members E2f7 and E2f8 is essential for murine embryonic developm

27 A deficiency in E2f7 and E2f8 led to an increase in E2f1 and p53, as wel

28 stems from a negative feedback loop in which E2F7 and E2F8 limit the expression of E2F1 and prevent E

29 Interestingly, E2F7 and E2F8 share unique structural features that dist

30 Homo- and heterodimers of E2F7 and E2F8 were found on target promoters, including

31 mice identified a set of shared targets for E2F7 and E2F8 whose increased expression during early po

32 Atypical E2F transcription factors (E2F7 and E2F8) function as key regulators of cell cycle

33 opmental Cell) shows that the atypical E2Fs, E2F7 and E2F8, are critical for mouse development.

34 skin cancer, the role of the atypical E2Fs, E2F7 and E2F8, in keratinocyte homeostasis, regeneration

35 enes, the atypical E2F transcription factors E2f7 and E2f8, were most highly upregulated in miR-142-d

36 We now find that E2F7 and E2F8, which are induced by E2F1-3 at G1/S, can

37 two most recently discovered mammalian E2Fs-E2F7 and E2F8.

38 tion of cell cycle-related genes, with E2F6, E2F7, and E2F8 playing key roles in repression.

39 These findings identify E2F7 as a novel member of the mammalian E2F transcriptio

40 We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently up-re

41 gene after genotoxic stress, consistent with E2F7 being a novel p53 target.

42 The transcription factors RB, E2F1 and E2F7 bind to a subset of DREAM target genes that functio

43 Once induced, E2F7 binds and represses a series of E2F target genes an

44 In response to cellular DNA damage, E2F7, but not E2F6 or E2F8, is up-regulated in a p53-dep

45 In contrast to the E2F activators, E2F7 can block the E2F-dependent activation of a subset

46 Mechanistically, E2F7 compensates for the loss of RB in repressing mitoti

47 assays demonstrate the formation of an E2F1-E2F7 complex, as well as an E2F7-E2F7 complex on adjacen

48 In turn, this E2F7-dependent mechanism contributes to p53-dependent ce

49 ation of an E2F1-E2F7 complex, as well as an E2F7-E2F7 complex on adjacent E2F-binding sites.

50 ntal lineage-specific cre mice, we show that E2F7/E2F8 functions in extraembryonic trophoblast lineag

51 ator as a key family member that antagonizes E2F7/E2F8 functions.

52 cental defects, and fostered the survival of E2f7/E2f8-deficient embryos to birth.

53 Ablation of E2F7 expression abrogates p53-dependent repression of a

54 Indeed, p53 occupies the promoter of the E2F7 gene after genotoxic stress, consistent with E2F7 b

55 First, the E2F7 gene encodes a protein that possesses two distinct

56 ther, our results identify a causal role for E2F7 in cellular senescence and uncover a novel link bet

57 ors, E2F1, E2F2, and E2F3, the expression of E2F7 is growth-regulated, at least in part, through E2F

58 HFR promoters is detected, and expression of E2F7 is sufficient to inhibit cell proliferation.

59 transcriptional up-regulation of its target, E2F7, leads to repression of relevant gene expression.

60 Furthermore, E2F7 occupancy of the E2F1 and DHFR promoters is detecte

61 Similar to E2F7, overexpression of E2F8 significantly slows down th

62 We also show that E2F7 recruits the co-repressor C-terminal-binding protei

63 otein (CtBP) and that CtBP2 is essential for E2F7 to repress E2F1 transcription.

64 ruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that