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E2F4 transcriptional repressor physically associates to the VHL demethylated promoter. These observations together with the finding of elevated E2F4 levels in early-onset preeclampsia (E-PE) placentae suggest that E2F4 inactivates VHL gene expression in E-PE due to enhanced binding to the VHL promoter as a consequence of the reduced methylation status of its binding site.
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HSP27 promotes cell cycle progression of MRC-5 cells by suppressing expression of the transcriptional repressors E2F-4 and p130
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E2f4 forms apical cytoplasmic organizing centres for assembly and nucleation of deuterosomes. Using genetically altered mice and E2F4 mutant proteins we demonstrate that centriole amplification is crucially dependent on these organizing centres and that, without cytoplasmic E2f4, deuterosomes are not assembled, halting multiciliogenesis
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Studied expression of E2F4 in breast cancer patients undergoing neoadjuvant chemotherapy; found target gene-based signature of E2F4 can be used to predict neoadjuvant response.
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The authors found that phosphorylation of residues S650 and S975 in p107 weakens the E2F4 transactivation domain binding.
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E2F4 gene expression in glioblastoma.
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Integrative genomic analyses confirm that E2F4 or E2F1 expression level is high in liposarcoma patients which associate with unfavorable prognosis.
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This study found evidence that the number of triplet AGC repeats in the E2F4 gene may play a role in the susceptibility to early-onset colorectal cancer.
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PHF8 reduces the H3K9me2 level at the E2F4 transcriptional start site, demonstrating a direct function of PHF8 in endothelial E2F4 gene regulation
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cell cycle-dependent transcription of the TRAIP gene by E2F1, E2F2, and E2F4 and rapid protein degradation leads to cell cycle-dependent expression with a maximum in G2/M
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Authors show that BRCA1 and RAD17 genes, whose derived proteins play a pivotal role in DNA damage repair, are transcriptional targets of gain-of-function mutant p53 proteins.
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Data suggest that aberrant cell cycle activation in Ewing sarcoma is due to the de-repression of transcription factor E2F targets of transcriptional induction and physical recruitment of E2F3 by fusion protein EWS-FLI1 replacing E2F4 on their promoters.
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The inverse immunohistochemical relationship between E2F1 and E2F4 indicates a possible mechanistic interlink in colorectal cancer.
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E2F4 promoter occupancy is globally associated with p53-repression targets, but not with p53 activation targets.
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cancer-associated E2F4 mutations enhance the capacity of colorectal cancer cells to grow without anchorage, thereby contributing to tumor progression.
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Analysis data from a panel of cell cycle transcription factors (E2F1, E2F4, E2F6, and GABPA) finds that a set of core cell cycle genes regulated in both U2OS and HeLa cells are bound by multiple cell cycle transcription factors.
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Short alleles (<13 repeats) of (AGC)n in E2F4 were less frequent in women with breast cancer than in the control sample.
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the loss of CDH1/E2F4 may be associated with worse clinical and pathological findings in mammary ductal carcinoma.
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Trim28 regulates cell proliferation by bridging HDAC1 and E2F3 and E2F4 interactions.
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In terminally differentiated cells, common KDM5A and E2F4 gene targets were bound by the pRB-related protein p130, a DREAM complex component.
