Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP. - Wikidata - wikimedia - TriplyDB

Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.

Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.

http://www.wikidata.org/entity/Q33604848

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Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis Keeping it quiet: chromatin control of gammaherpesvirus latency Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis Epstein-Barr virus latent genes The EBNA3 family of Epstein-Barr virus nuclear proteins associates with the USP46/USP12 deubiquitination complexes to regulate lymphoblastoid cell line growth Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection Extensive co-operation between the Epstein-Barr virus EBNA3 proteins in the manipulation of host gene expression and epigenetic chromatin modification.Epigenetic markers for early detection of nasopharyngeal carcinoma in a high risk population.Loss of P16 Protein Expression and Its Association with Epstein-Barr Virus LMP-1 Expression in Hodgkin's Lymphoma Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.Epstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1 E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytes Epstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cells Functional modulation of the metastatic suppressor Nm23-H1 by oncogenic viruses Epstein-Barr virus nuclear antigen 3A partially coincides with EBNA3C genome-wide and is tethered to DNA through BATF complexes.Modulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming.Inactivation of intergenic enhancers by EBNA3A initiates and maintains polycomb signatures across a chromatin domain encoding CXCL10 and CXCL9 EBNA3C augments Pim-1 mediated phosphorylation and degradation of p21 to promote B-cell proliferation Epstein-Barr Virus Proteins EBNA3A and EBNA3C Together Induce Expression of the Oncogenic MicroRNA Cluster miR-221/miR-222 and Ablate Expression of Its Target p57KIP2.EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors.EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B Cells Comparative methylome analysis in solid tumors reveals aberrant methylation at chromosome 6p in nasopharyngeal carcinoma.Repression of Hox genes by LMP1 in nasopharyngeal carcinoma and modulation of glycolytic pathway genes by HoxC8.BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV Identification of MEF2B, EBF1, and IL6R as Direct Gene Targets of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Critical for EBV-Infected B-Lymphocyte Survival Metabolic stress is a barrier to Epstein-Barr virus-mediated B-cell immortalization.Epstein-Barr virus-induced epigenetic alterations following transient infection.Biochemical and functional interactions of human papillomavirus proteins with polycomb group proteins.Towards incorporating epigenetic mechanisms into carcinogen identification and evaluation.MYC activation and BCL2L11 silencing by a tumour virus through the large-scale reconfiguration of enhancer-promoter hubs.Epstein-Barr virus induces global changes in cellular mRNA isoform usage that are important for the maintenance of latency.Epstein-Barr virus nuclear antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.Epstein-Barr virus super-enhancer eRNAs are essential for MYC oncogene expression and lymphoblast proliferation Epigenetic reprogramming of host genes in viral and microbial pathogenesis Tumor viruses and cancer biology: Modulating signaling pathways for therapeutic intervention.Epstein-Barr virus genetics: talking about the BAC generation.

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Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.

http://www.wikidata.org/entity/Q33604848

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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type

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Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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prefLabel

Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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Epigenetic repression of p16(I ...... f EBNA3A and EBNA3C with CtBP.

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Lenka Skalska

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Martin J Allday

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Melanie Franz

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Michaela Ruhmann

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P2860

The Polycomb group protein EZH2 directly controls DNA methylation

Molecular cloning and characterization of a cellular phosphoprotein that interacts with a conserved C-terminal domain of adenovirus E1A involved in negative modulation of oncogenic transformation

Epstein-Barr virus nuclear antigen 3C interacts with and enhances the stability of the c-Myc oncoprotein

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

Histone demethylation mediated by the nuclear amine oxidase homolog LSD1

Epstein-Barr virus latent antigen 3C can mediate the degradation of the retinoblastoma protein through an SCF cellular ubiquitin ligase

C-Terminal binding protein is a transcriptional repressor that interacts with a specific class of vertebrate Polycomb proteins

SCFSkp2 complex targeted by Epstein-Barr virus essential nuclear antigen

Epigenetic transcriptional repression of cellular genes by a viral SET protein

Histone demethylase JMJD3 contributes to epigenetic control of INK4a/ARF by oncogenic RAS

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20548956

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Epstein–Barr virus

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2883600

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