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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  WT p53 directly inhibits ATX expression via E2F7.
6 tocol revealed that combined inactivation of E2f7/8 enhanced tumorigenesis and accelerated malignant
7  Caenorhabditis elegans, we identify a novel E2F7/8 homolog, EFL-3, and show that EFL-3 functions coo
8 ndicating that the tumor-promoting effect of E2F7/8 inactivation can be partially compensated via E2F
9 -deficient neoplastic cells, indicating that E2F7/8 might inhibit intratumoral vessel branching via i
10 chanism of the tumor suppressor functions of E2F7/8 remain obscure.
11                                 Importantly, E2F7/8 repressed a large set of E2F target genes that ar
12                         We show that loss of E2F7/8 triggers apoptosis via induction of E2F1 in respo
13 hanced intratumoral branching in xenografted E2f7/8-deficient neoplasms compared with E2f7/8-proficie
14 itor of vascular branching, was decreased in E2f7/8-deficient neoplastic cells, indicating that E2F7/
15 or successful isolation and establishment of E2f7/8-deficient primary keratinocyte cultures was much
16                                    Moreover, E2f7/8-deficient primary keratinocytes proliferate more
17 ted E2f7/8-deficient neoplasms compared with E2f7/8-proficient neoplasms.
18 risingly, concomitant inactivation of Rb and E2f7, a close family member of E2f8, did not substantial
19                                              E2F7, a transcriptional regulator of canonical S-to-G2 p
20 ine-controlled transcriptional activation of E2f7 and E2f8 and induced their expression during postna
21                       These results identify E2F7 and E2F8 as a unique repressive arm of the E2F tran
22 se observations, together with the fact that E2F7 and E2F8 can homodimerize and are expressed in the
23                                          The E2f7 and E2f8 family members are thought to function as
24 the function of the atypical repressor genes E2f7 and E2f8 in adult liver physiology.
25 ice, we determined that combined deletion of E2f7 and E2f8 in hepatocytes leads to HCC.
26 ve analyzed the consequences of inactivating E2f7 and E2f8 in mice and show that their individual los
27 prisingly, keratinocyte-specific deletion of E2F7 and E2F8 in mice did not interfere with skin develo
28 nce-mediated (CRISPRi-mediated) silencing of E2F7 and E2F8 in miR-142-deficient T cells ameliorated c
29                                 Mice lacking E2f7 and E2f8 in the liver (liver-specific E2f7/E2f8 kno
30 dy, aneuploidy, and adaptation, mice lacking E2f7 and E2f8 in the liver (LKO), which have a polyploid
31                      In adult mice, however, E2F7 and E2F8 induction was well tolerated, yet profound
32 ctors consisting of the two atypical members E2f7 and E2f8 is essential for murine embryonic developm
33                              A deficiency in E2f7 and E2f8 led to an increase in E2f1 and p53, as wel
34 stems from a negative feedback loop in which E2F7 and E2F8 limit the expression of E2F1 and prevent E
35               The physiological relevance of E2F7 and E2F8 remains incompletely understood, largely b
36                               Interestingly, E2F7 and E2F8 share unique structural features that dist
37                    Homo- and heterodimers of E2F7 and E2F8 were found on target promoters, including
38  mice identified a set of shared targets for E2F7 and E2F8 whose increased expression during early po
39          Atypical E2F transcription factors (E2F7 and E2F8) function as key regulators of cell cycle
40 opmental Cell) shows that the atypical E2Fs, E2F7 and E2F8, are critical for mouse development.
41               Two members of the E2F family, E2F7 and E2F8, are potent repressors of E2F-dependent tr
42  in particular activator E2F1 and repressors E2F7 and E2F8, form a feedback circuit at the crossroads
43  skin cancer, the role of the atypical E2Fs, E2F7 and E2F8, in keratinocyte homeostasis, regeneration
44        However, atypical repressors, such as E2F7 and E2F8, lack DP interaction domains and their fun
45 at mitosis by the transcriptional repressors E2F7 and E2F8, leading to formation of polyploid cells.
46  protein directly represses transcription of E2f7 and E2f8, thereby promoting mitosis.
47 enes, the atypical E2F transcription factors E2f7 and E2f8, were most highly upregulated in miR-142-d
48                             We now find that E2F7 and E2F8, which are induced by E2F1-3 at G1/S, can
49 mplex/cyclosome (APC/C), which also controls E2F7 and E2F8.
50  two most recently discovered mammalian E2Fs-E2F7 and E2F8.
51 t is dependent on the atypical E2F proteins, E2F7 and E2F8.
52                        Systemic induction of E2f7 and, to lesser extent, E2f8 transgenes in juvenile
53 tion of cell cycle-related genes, with E2F6, E2F7, and E2F8 playing key roles in repression.
54                      These findings identify E2F7 as a novel member of the mammalian E2F transcriptio
55   We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently up-re
56 gene after genotoxic stress, consistent with E2F7 being a novel p53 target.
57       The transcription factors RB, E2F1 and E2F7 bind to a subset of DREAM target genes that functio
58 t chromosome looping brings together the two E2F7 binding sites.
59                                Once induced, E2F7 binds and represses a series of E2F target genes an
60          In response to cellular DNA damage, E2F7, but not E2F6 or E2F8, is up-regulated in a p53-dep
61           In contrast to the E2F activators, E2F7 can block the E2F-dependent activation of a subset
62                                      Loss of E2F7 causes aberrant acquisition of DNA synthesis in mul
63                             Mechanistically, E2F7 compensates for the loss of RB in repressing mitoti
64 n contrast, an atypical transcription factor E2F7 competed against DP1 and blocked E2F1-induced KPNA2
65  assays demonstrate the formation of an E2F1-E2F7 complex, as well as an E2F7-E2F7 complex on adjacen
66                                In turn, this E2F7-dependent mechanism contributes to p53-dependent ce
67                 In the multiciliation cycle, E2F7 directly dampens the expression of genes encoding D
68 ation of an E2F1-E2F7 complex, as well as an E2F7-E2F7 complex on adjacent E2F-binding sites.
69 entially confounding effects associated with E2f7/E2f8 deficiency.
70 ntal lineage-specific cre mice, we show that E2F7/E2F8 functions in extraembryonic trophoblast lineag
71 ator as a key family member that antagonizes E2F7/E2F8 functions.
72 g E2f7 and E2f8 in the liver (liver-specific E2f7/E2f8 knockout; LKO) were recently reported to have
73 cental defects, and fostered the survival of E2f7/E2f8-deficient embryos to birth.
74  and cell cycle progression by relieving the E2F7/E2F8-mediated inhibition is unknown.
75                                  Ablation of E2F7 expression abrogates p53-dependent repression of a
76 fied GRNs for five transcription regulators: E2f7, Gbx1, Sox10, Prox1, and Onecut2, which play crucia
77     Indeed, p53 occupies the promoter of the E2F7 gene after genotoxic stress, consistent with E2F7 b
78                                   First, the E2F7 gene encodes a protein that possesses two distinct
79               We report here that EFL-3, the E2F7 homologue of Caenorhabditis elegans, regulates epid
80 ther, our results identify a causal role for E2F7 in cellular senescence and uncover a novel link bet
81                                  In summary, E2F7 is a common transcription factor that upregulates A
82 ors, E2F1, E2F2, and E2F3, the expression of E2F7 is growth-regulated, at least in part, through E2F
83 HFR promoters is detected, and expression of E2F7 is sufficient to inhibit cell proliferation.
84 transcriptional up-regulation of its target, E2F7, leads to repression of relevant gene expression.
85                 Binding of p53 disrupted the E2F7-mediated chromosomal looping and repressed Enpp2 tr
86       In contrast, we found no disruption of E2F7-mediated ENPP2 transcription via direct p53 binding
87  expression of BRCA2, a target of CHEK2-TP53-E2F7-mediated transcriptional repression.
88                                 Furthermore, E2F7 occupancy of the E2F1 and DHFR promoters is detecte
89 of E2F1 abolished the suppressive effects of E2F7 on KPNA2 gene expression.
90     Mutation of the dimerization residues of E2F7 or DNA-binding domain of E2F1 abolished the suppres
91                                   Similar to E2F7, overexpression of E2F8 significantly slows down th
92 d chromosome immunoprecipitation showed that E2F7 promotes Enpp2 transcription through cooperative bi
93 ng/blocking of the transcriptional repressor E2F7, promoting transcription of key genes that stimulat
94 sm of YAP transcription regulation involving E2F7, RCOR, and Sin3 HDAC.
95                            We also show that E2F7 recruits the co-repressor C-terminal-binding protei
96                                 Knockdown of E2F7 reduced ATX expression and chromosome immunoprecipi
97 scription through cooperative binding to two E2F7 sites (promoter region -1393 bp and second intron 9
98 otein (CtBP) and that CtBP2 is essential for E2F7 to repress E2F1 transcription.
99 A2 mediated nuclear localization of E2F1 and E2F7, where they in turn controlled KPNA2 expression.
100 ruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that
101 ributes to YAP transcriptional silencing via E2F7, which recruits the RCOR co-repressor complex to YA

 
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