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E2F transcription factor 4, p107/p130-binding

The protein encoded by this gene is a member of the E2F family of transcription factors. The E2F family plays a crucial role in the control of cell cycle and action of tumor suppressor proteins and is also a target of the transforming proteins of small DNA tumor viruses. The E2F proteins contain several evolutionally conserved domains found in most members of the family. These domains include a DNA binding domain, a dimerization domain which determines interaction with the differentiation regulated transcription factor proteins (DP), a transactivation domain enriched in acidic amino acids, and a tumor suppressor protein association domain which is embedded within the transactivation domain. This protein binds to all three of the tumor suppressor proteins pRB, p107 and p130, but with higher affinity to the last two. It plays an important role in the suppression of proliferation-associated genes, and its gene mutation and increased expression may be associated with human cancer. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: E2F1, CD43, PCNA, p107, pRb
Papers using E2F4 antibodies
DBTSS: database of transcription start sites, progress report 2008.
Patil Christopher K., In PLoS ONE, 2007
... pre-incubated with either 10 µg RNA polymerase II antibody (Abcam, Cambridge, MA) or 10 µg E2F-4 antibody (Santa Cruz Biotechnology, Santa Cruz, CA) ...
DNA binding sites: representation and discovery.
Fairhead Cecile, In PLoS ONE, 1999
... E2F4 antisera were obtained from Santa Cruz Biotechnology (polyclonal, rabbit, sc-1082) and ...
Papers on E2F4
Trinucleotide repeat expansions in human breast cancer-susceptibility genes: relevant targets for aspirin chemoprevention?
Tunalı et al., İstanbul, Turkey. In Clin Transl Oncol, Jan 2016
Nucleotide repeat expansions also exist in E2F4 and POLG genes in BC.
Dietary myo-inositol modulates immunity through antioxidant activity and the Nrf2 and E2F4/cyclin signalling factors in the head kidney and spleen following infection of juvenile fish with Aeromonas hydrophila.
Feng et al., Chengdu, China. In Fish Shellfish Immunol, Jan 2016
The oxidative damage due to MI deficiency also resulted in the inhibition of proliferation-associated signalling (cyclin D1, cyclin A, cyclin E and E2F4).
Indirect p53-dependent transcriptional repression of Survivin, CDC25C, and PLK1 genes requires the cyclin-dependent kinase inhibitor p21/CDKN1A and CDE/CHR promoter sites binding the DREAM complex.
Engeland et al., Leipzig, Germany. In Oncotarget, Jan 2016
Chromatin immunoprecipitation (ChIP) data indicate that promoter binding of B-MYB switches to binding of E2F4 and p130 resulting in a replacement of the MMB (Myb-MuvB) by the DREAM complex.
Characterization of the promoter region of the bovine long-chain acyl-CoA synthetase 1 gene: Roles of E2F1, Sp1, KLF15, and E2F4.
Zhang et al., China. In Sci Rep, Dec 2015
Mutational analysis and electrophoretic mobility shift assays demonstrated that E2F1, Sp1, KLF15 and E2F4 binding to the promoter region drives ACSL1 transcription.
The Histone Demethylase PHF8 Is Essential for Endothelial Cell Migration.
Fork et al., Frankfurt am Main, Germany. In Plos One, Dec 2015
Given the impact of PHF8 on cell cycle genes, endothelial E2F transcription factors were screened, which led to the identification of the gene repressor E2F4 to be controlled by PHF8.
Autophagy positively regulates DNA damage recognition by nucleotide excision repair.
He et al., Chicago, United States. In Autophagy, Dec 2015
First, autophagy deficiency downregulates the transcription of XPC through TWIST1-dependent activation of the transcription repressor complex E2F4-RBL2.
In vivo genome-wide binding of Id2 to E2F4 target genes as part of a reversible program in mice liver.
García-Trevijano et al., Valencia, Spain. In Cell Mol Life Sci, 2014
Id2 and E2F4 are known to bind simultaneously to c-myc promoter.
The DREAM complex in antitumor activity of imatinib mesylate in gastrointestinal stromal tumors.
Duensing et al., Pittsburgh, United States. In Curr Opin Oncol, 2014
Mechanistically, this process involves the DREAM complex (DP, p130/RBL2, E2F4 and MuvB), a newly identified key regulator of quiescence.
Activity, regulation, copy number and function in the glyoxalase system.
Thornalley et al., Coventry, United Kingdom. In Biochem Soc Trans, 2014
Human GLO1 has MRE (metal-response element), IRE (insulin-response element), E2F4 (early gene 2 factor isoform 4), AP-2α (activating enhancer-binding protein 2α) and ARE (antioxidant response-element) regulatory elements and is a hotspot for copy number variation.
p27(Kip1) directly represses Sox2 during embryonic stem cell differentiation.
Serrano et al., Madrid, Spain. In Cell Stem Cell, 2013
Mechanistically, we have found that upon differentiation p27 associates to the SRR2 enhancer of the Sox2 gene together with a p130-E2F4-SIN3A repressive complex.
Induction of Wnt/β-catenin signaling in mouse mesenchymal stem cells is associated with activation of the p130 and E2f4 and formation of the p130/Gsk3β/β-catenin complex.
Popov et al., Saint Petersburg, Russia. In Stem Cells Dev, 2012
Induction of Wnt/beta-catenin signaling in mouse mesenchymal stem cells is associated with activation of the p130 and E2f4 and formation of the p130/Gsk3beta/beta-catenin complex.
Unraveling the genetics of otitis media: from mouse to human and back again.
Jamieson et al., Australia. In Mamm Genome, 2011
Single-gene mouse mutants with OM have identified a number of genes, namely, Eya4, Tlr4, p73, MyD88, Fas, E2f4, Plg, Fbxo11, and Evi1, as potential and biologically relevant candidates for human disease.
An integrated bioinformatics approach identifies elevated cyclin E2 expression and E2F activity as distinct features of tamoxifen resistant breast tumors.
Dai et al., Chicago, United States. In Plos One, 2010
Tamoxifen resistant tumors displayed enriched expression of genes related to cell cycle and proliferation, as well as elevated activity of E2F transcription factors.
Disruption of calvarial ossification in E2f4 mutant embryos correlates with increased proliferation and progenitor cell populations.
Lees et al., Cambridge, United States. In Cell Cycle, 2010
E2F4 plays an important role in enabling osteoblast progenitors to exit the cell cycle and subsequently differentiate thereby contributing to the commitment of these cells to the bone lineage.
E2F4 is required for cardiomyocyte proliferation.
Engel et al., Bad Nauheim, Germany. In Cardiovasc Res, 2010
Our data indicate that E2F4 is required for cardiomyocyte proliferation and suggest a function for E2F4 in mitosis
pRB and E2F4 play distinct cell-intrinsic roles in fetal erythropoiesis.
Lees et al., Cambridge, United States. In Cell Cycle, 2010
E2F4 controls cell cycle exit through different mechanisms.
C/EBPbeta at the core of the TGFbeta cytostatic response and its evasion in metastatic breast cancer cells.
Massagué et al., New York City, United States. In Cancer Cell, 2006
We found the transcription factor C/EBPbeta to be essential for TGFbeta induction of the cell cycle inhibitor p15INK4b by a FoxO-Smad complex and repression of c-MYC by an E2F4/5-Smad complex in human epithelial cells.
Prediction of preadipocyte differentiation by gene expression reveals role of insulin receptor substrates and necdin.
Kahn et al., Boston, United States. In Nat Cell Biol, 2005
Insulin receptor substrate proteins regulate a necdin-E2F4 interaction that represses peroxisome-proliferator-activated receptor gamma (PPARgamma) transcription via a cyclic AMP response element binding protein (CREB)-dependent pathway.
Mapping DNA-protein interactions in large genomes by sequence tag analysis of genomic enrichment.
Iyer et al., Austin, United States. In Nat Methods, 2005
We used STAGE to identify several previously unknown binding targets of human transcription factor E2F4 that we independently validated by promoter-specific PCR and microarray hybridization.
Aging reduces proliferative capacities of liver by switching pathways of C/EBPalpha growth arrest.
Timchenko et al., Houston, United States. In Cell, 2003
We identified an age-specific C/EBPalpha-Rb-E2F4 complex that binds to E2F-dependent promoters and represses these genes.
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