Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression. - Wikidata - wikimedia - TriplyDB

Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.

Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.

http://www.wikidata.org/entity/Q34549944

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Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis Potential cellular functions of Epstein-Barr Nuclear Antigen 1 (EBNA1) of Epstein-Barr Virus 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.Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.Epstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.The effect of Epstein-Barr virus Latent Membrane Protein 2 expression on the kinetics of early B cell infection 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 Epstein-Barr virus-positive T/NK-cell lymphoproliferative disorders 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.Epstein-Barr virus oncoprotein super-enhancers control B cell growth Epigenetic silencing of tumor suppressor genes during in vitro Epstein-Barr virus infection.Cyclin D1 overexpression supports stable EBV infection in nasopharyngeal epithelial cells Epstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic Sites Towards incorporating epigenetic mechanisms into carcinogen identification and evaluation.Epstein-Barr virus induces global changes in cellular mRNA isoform usage that are important for the maintenance of latency.Epstein-Barr virus nuclear antigen leader protein localizes to promoters and enhancers with cell transcription factors and EBNA2.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 Inhibition of germinal centre apoptotic programmes by epstein-barr virus.Epigenomic deregulation in the immune system.Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.EBV finds a polycomb-mediated, epigenetic solution to the problem of oncogenic stress responses triggered by infection Switching of EBV cycles between latent and lytic states.Dynamic Epstein-Barr virus gene expression on the path to B-cell transformation.Modes of infection and oncogenesis by the Epstein-Barr virus.Role of epigenetics in EBV regulation and pathogenesis.Epstein-Barr virus infection and persistence in nasopharyngeal epithelial cells.The Epstein-Barr virus and the pathogenesis of lymphoma.At a crossroads: human DNA tumor viruses and the host DNA damage response.EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.

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Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.

http://www.wikidata.org/entity/Q34549944

description

2011 nî lūn-bûn

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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type

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

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PNAS.1019599108

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Epstein-Barr virus nuclear ant ...... 16INK4A and p14ARF expression.

@en

P2093

Bo Zhao

http://www.w3.org/2001/XMLSchema#string

Eric Johannsen

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James Zou

http://www.w3.org/2001/XMLSchema#string

Kenzo Takada

http://www.w3.org/2001/XMLSchema#string

Seiji Maruo

http://www.w3.org/2001/XMLSchema#string

P2860

Characterization of DP103, a novel DEAD box protein that binds to the Epstein-Barr virus nuclear proteins EBNA2 and EBNA3C

The amino-terminal domains of Epstein-Barr virus nuclear proteins 3A, 3B, and 3C interact with RBPJ(kappa)

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

Epstein-Barr virus nuclear antigen 3C and prothymosin alpha interact with the p300 transcriptional coactivator at the CH1 and CH3/HAT domains and cooperate in regulation of transcription and histone acetylation.

Epstein-Barr virus nuclear antigen 3C putative repression domain mediates coactivation of the LMP1 promoter with EBNA-2.

SCFSkp2 complex targeted by Epstein-Barr virus essential nuclear antigen

Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands

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

A conserved domain of the Epstein-Barr virus nuclear antigens 3A and 3C binds to a discrete domain of Jkappa

Modulation of histone acetyltransferase activity through interaction of epstein-barr nuclear antigen 3C with prothymosin alpha

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1919-1924

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scholarly article

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10.1073/PNAS.1019599108

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5

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108

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Elliott D. Kieff

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2011-01-18T00:00:00Z

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49765309

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21245331

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Epstein–Barr virus

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3033265

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