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E2F transcription factor 6

This gene encodes a member of the E2F transcription factor protein family. E2F family members play a crucial role in control of the cell cycle and of the action of tumor suppressor proteins. They are also a target of the transforming proteins of small DNA tumor viruses. Many E2F proteins contain several evolutionarily conserved domains: 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. The encoded protein of this gene is atypical because it lacks the transactivation and tumor suppressor protein association domains. It contains a modular suppression domain and is an inhibitor of E2F-dependent transcription. The protein is part of a multimeric protein complex that contains a histone methyltransferase and the transcription factors Mga and Max. Multiple transcript variants have been reported for this gene, but it has not been clearly demonstrated that they encode valid isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: E2F1, E2F4, CAN, Polycomb, Histone
Papers on E2F6
Interplay between the E2F pathway and β-adrenergic signaling in the pathological hypertrophic response of myocardium.
Tuana et al., Ottawa, Canada. In J Mol Cell Cardiol, Jul 2015
We previously examined this pathway in the myocardium via manipulation of the unique E2F repressor, E2F6, which is believed to repress gene activity independently of Rb.
Oct3/4 directly regulates expression of E2F3a in mouse embryonic stem cells.
Koide et al., Kanazawa, Japan. In Biochem Biophys Res Commun, May 2015
Suppression of E2F3a activity by E2F6 overexpression led to the reduced proliferation in ES cells, which was relieved by co-expression of E2F3a.
miR-185 suppresses tumor proliferation by directly targeting E2F6 and DNMT1 and indirectly upregulating BRCA1 in triple-negative breast cancer.
Xie et al., Guangzhou, China. In Mol Cancer Ther, 2014
We further identified that miR-185 directly targeted DNMT1 and E2F6, which resulted in a marked increase in the expression of BRCA1 at the mRNA and protein levels in TNBC.
Regulation of microRNA-mediated gene silencing by microRNA precursors.
Kay et al., Stanford, United States. In Nat Struct Mol Biol, 2014
We show that mouse pri- or pre-miR-151 can bind to and compete with mature miR-151-5p and miR-151-3p for binding sites contained within the complementary regions of the E2f6 mRNA 3' untranslated region (UTR).
Promising roles of mammalian E2Fs in hepatocellular carcinoma.
Li et al., Hefei, China. In Cell Signal, 2014
Eight members, E2F1 E2F8 have been recognized of this family so far, and the members of this family are generally divided into activator E2F (E2F1--E2F3a), repressor E2F (E2F3b--E2F5) and inhibitor E2F (E2F6--E2F8) subclasses based on their structur-e and function.
Bortezomib effect on E2F and cyclin family members in human hepatocellular carcinoma cell lines.
Grassi et al., Trieste, Italy. In World J Gastroenterol, 2014
As observed with JHH6, BZB treatment of HepG2 cells induced a significant increase in mRNA levels of an anti-proliferative E2F member, E2F6 in this case.
A mathematical model of bimodal epigenetic control of miR-193a in ovarian cancer stem cells.
Chan et al., Zhengzhou, China. In Plos One, 2013
To unravel this complexity, we propose a mathematical model to explore how estrogen-mediated up-regulation of another target of miR-193a, namely E2F6, can attenuate the function of miR-193a in two ways, one through a competition of E2F6 and c-KIT transcripts for miR-193a, and second by binding of E2F6 protein, in association with a polycomb complex, to the promoter of miR-193a to down-regulate its transcription.
Polycomb protein EZH2 suppresses apoptosis by silencing the proapoptotic miR-31.
Guo et al., Fargo, United States. In Cell Death Dis, 2013
SiRNA knockdown of EZH2 increased miR-31 expression and decreased the antiapoptotic protein E2F6 (E2F transcription factor 6) (a target of miR-31), resulting in the sensitization of prostate cancer cells to docetaxel-induced apoptosis.
Cross-species transcriptomic analysis elucidates constitutive aryl hydrocarbon receptor activity.
Boutros et al., Toronto, Canada. In Bmc Genomics, 2013
RESULTS: We found significantly more overlap in constitutive mRNA abundances amongst tissues within the same species than from tissues between species and identified 13 genes (Agt, Car3, Creg1, Ctsc, E2f6, Enpp1, Gatm, Gstm4, Kcnj8, Me1, Pdk1, Slc35a3, and Sqrdl) that are affected by AHR-status in four of five tissues.
Transcriptional regulation and spatial interactions of head-to-head genes.
Li et al., Shanghai, China. In Bmc Genomics, 2013
Factors such as HEY1, GABP, Sin3Ak-20, POL2, E2F6, and c-MYC are essential for the bidirectional transcription of intra-H2H pairs; while factors like CTCF, BDP1, GATA2, RAD21, and POL3 play important roles in coherently regulating inter-H2H pairs; iii) H2H gene blocks are enriched with hypersensitive DNase and modified histones, which participate in active transcriptions; and iv) H2H genes tend to be highly connected compared with non-H2H genes in the human co-expression network.
HOXC9 directly regulates distinct sets of genes to coordinate diverse cellular processes during neuronal differentiation.
Ding et al., Augusta, United States. In Bmc Genomics, 2012
Moreover, we showed that HOXC9 interacted with the transcriptional repressor E2F6 and recruited it to the promoters of cell cycle genes for repressing their expression.
Pathway Analysis of ChIP-Seq-Based NRF1 Target Genes Suggests a Logical Hypothesis of their Involvement in the Pathogenesis of Neurodegenerative Diseases.
Yamamoto et al., Tokyo, Japan. In Gene Regul Syst Bio, 2012
The set of ChIP-Seq-based NRF1 target genes included known NRF1 targets such as EIF2S1, EIF2S2, CYCS, FMR1, FXR2, E2F6, CD47, and TOMM34.
A novel in silico reverse-transcriptomics-based identification and blood-based validation of a panel of sub-type specific biomarkers in lung cancer.
Liloglou et al., In Bmc Genomics, 2012
Our results suggest that overexpression of HMGA1, E2F6, IRF1, and TFDP1 and downregulation or no expression of SUV39H1, RBL1, and HNRPD in blood is suitable for diagnosis of lung adenocarcinoma and squamous cell carcinoma sub-types of NSCLC.
The polycomb group protein L3mbtl2 assembles an atypical PRC1-family complex that is essential in pluripotent stem cells and early development.
Hock et al., Boston, United States. In Cell Stem Cell, 2012
L3mbtl2 regulates genes by recruiting a Polycomb Repressive Complex1 (PRC1)-related complex, resembling the previously described E2F6-complex, and including G9A, Hdac1, and Ring1b.
A conserved E2F6-binding element in murine meiosis-specific gene promoters.
Terada et al., Gainesville, United States. In Biol Reprod, 2008
possesses a broad ability to bind to and regulate the meiosis-specific gene population
E2F6 inhibits cobalt chloride-mimetic hypoxia-induced apoptosis through E2F1.
Yang et al., Shanghai, China. In Mol Biol Cell, 2008
E2F6 has a role in control of hypoxia-induced apoptosis through regulation of E2F1
E2f6 and Bmi1 cooperate in axial skeletal development.
Lees et al., Cambridge, United States. In Dev Dyn, 2008
This analysis shows that E2f6 and Bmi1 cooperate in the regulation of Hox genes, and consequently axial skeleton development, but not in the repression of the Ink4a-Arf locus.
Analysis of the relevance of e2fs and their target genes with rat liver regeneration.
Xu et al., In Indian J Gastroenterol, 2008
E2F transcription factor genes and their 34 target genes have a role in liver regeneration.
A comprehensive ChIP-chip analysis of E2F1, E2F4, and E2F6 in normal and tumor cells reveals interchangeable roles of E2F family members.
Farnham et al., Davis, United States. In Genome Res, 2007
E2F6 binding sites are located within 2 kb of a transcription start site, in both normal and tumor cells
A complex with chromatin modifiers that occupies E2F- and Myc-responsive genes in G0 cells.
Nakatani et al., Boston, United States. In Science, 2002
data suggest that E2F- and Myc-responsive genes are coregulated by E2F6 complex in quiescent cells
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