Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim - Test2 - elhamkhani - TriplyDB

Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim

Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim

http://www.wikidata.org/entity/Q33474807

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The Modulation of Apoptotic Pathways by Gammaherpesviruses Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis Regulation of Bim in Health and Disease Early-life exposures to infectious agents and later cancer development Homeostasis and function of regulatory T cells in aging Epigenetic impact of infection on carcinogenesis: mechanisms and applications Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis Epstein-Barr virus latent genes The Epstein-Barr Virus (EBV) in T Cell and NK Cell Lymphomas: Time for a Reassessment.Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.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.Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Epstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1 Epstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.Epigenetic silencing of Bim transcription by Spi-1/PU.1 promotes apoptosis resistance in leukaemia Epstein-Barr virus nuclear antigen 3C regulated genes in lymphoblastoid cell lines.Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.A major role for Bim in regulatory T cell homeostasis.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 Expression of dual-specificity phosphatase 5 pseudogene 1 (DUSP5P1) in tumor cells Epstein-Barr virus down-regulates tumor suppressor DOK1 expression.EBNA3C augments Pim-1 mediated phosphorylation and degradation of p21 to promote B-cell proliferation Viral epigenetics.EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors.The Epstein-Barr Virus BART microRNAs target the pro-apoptotic protein Bim.Hypermethylation of the tumor suppressor gene PRDM1/Blimp-1 supports a pathogenetic role in EBV-positive Burkitt lymphoma.BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells.Epstein-Barr virus-induced epigenetic alterations following transient infection.Epigenetic silencing of the proapoptotic gene BIM in anaplastic large cell lymphoma through an MeCP2/SIN3a deacetylating complex.The B cell transcription program mediates hypomethylation and overexpression of key genes in Epstein-Barr virus-associated proliferative conversion.Epstein-Barr virus maintains lymphomas via its miRNAs.IL-15 Fosters Age-Driven Regulatory T Cell Accrual in the Face of Declining IL-2 Levels.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.Higher methylation intensity induced by EBV LMP1 via NF-κB/DNMT3b signaling contributes to silencing of PTEN gene Epstein-Barr virus nuclear antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.

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Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim

http://www.wikidata.org/entity/Q33474807

description

2009 nî lūn-bûn

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2009 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի հունիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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Epstein-barr virus latency in ...... the tumour suppressor gene Bim

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JOURNAL.PPAT.1000492

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Epstein-barr virus latency in ...... the tumour suppressor gene Bim

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Emma Anderton

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Kostas Paschos

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Martin J Allday

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Paul Smith

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P2860

Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals

The Polycomb group protein EZH2 directly controls DNA methylation

A degradation signal located in the C-terminus of p21WAF1/CIP1 is a binding site for the C8 alpha-subunit of the 20S proteasome

Counterregulation of chromatin deacetylation and histone deacetylase occupancy at the integrated promoter of human immunodeficiency virus type 1 (HIV-1) by the HIV-1 repressor YY1 and HIV-1 activator Tat

Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters

Lymphoproliferative disease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes

Epstein-Barr virus and Burkitt lymphoma

Host epigenetic modifications by oncogenic viruses

BAX activation is initiated at a novel interaction site

Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1

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6

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Jaap M Middeldorp

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26321421

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19557159

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Epstein–Barr virus

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