Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells. - Wikidata - wikimedia - TriplyDB

Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells.

Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells.

http://www.wikidata.org/entity/Q35540042

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Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis Role of Viral miRNAs and Epigenetic Modifications in Epstein-Barr Virus-Associated Gastric Carcinogenesis 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.Epigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.Extensive co-operation between the Epstein-Barr virus EBNA3 proteins in the manipulation of host gene expression and epigenetic chromatin modification.Mangiferin facilitates islet regeneration and β-cell proliferation through upregulation of cell cycle and β-cell regeneration regulators.Epstein-Barr virus nuclear antigen 3C facilitates G1-S transition by stabilizing and enhancing the function of cyclin D1.Unexpected instability of family of repeats (FR), the critical cis-acting sequence required for EBV latent infection, in EBV-BAC systems.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 Burkitt lymphoma: pathogenesis and immune evasion.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.Epstein-Barr virus nuclear antigen 3C regulated genes in lymphoblastoid cell lines.The effect of Epstein-Barr virus Latent Membrane Protein 2 expression on the kinetics of early B cell infection Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.The EBV Latent Antigen 3C Inhibits Apoptosis through Targeted Regulation of Interferon Regulatory Factors 4 and 8.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 nuclear protein 3C binds to the N-terminal (NTD) and beta trefoil domains (BTD) of RBP/CSL; only the NTD interaction is essential for lymphoblastoid cell growth.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.Epstein-Barr virus oncoprotein super-enhancers control B cell growth BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV EBV-encoded EBNA-6 binds and targets MRS18-2 to the nucleus, resulting in the disruption of pRb-E2F1 complexes Metabolic stress is a barrier to Epstein-Barr virus-mediated B-cell immortalization.Regulation of the retinoblastoma proteins by the human herpesviruses.Epstein-Barr virus nuclear protein EBNA3C residues critical for maintaining lymphoblastoid cell growth.MYC activation and BCL2L11 silencing by a tumour virus through the large-scale reconfiguration of enhancer-promoter hubs.Differential gene expression patterns of EBV infected EBNA-3A positive and negative human B lymphocytes.Epstein-Barr virus nuclear protein 3C domains necessary for lymphoblastoid cell growth: interaction with RBP-Jkappa regulates TCL1.Nucleoside diphosphate kinase/Nm23 and Epstein-Barr virus.Epstein-Barr virus nuclear antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.How does Epstein-Barr virus (EBV) complement the activation of Myc in the pathogenesis of Burkitt's lymphoma?Using Epstein-Barr viral load assays to diagnose, monitor, and prevent posttransplant lymphoproliferative disorder.Epstein-Barr virus genetics: talking about the BAC generation.

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Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells.

http://www.wikidata.org/entity/Q35540042

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2006 nî lūn-bûn

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2006 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

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2006 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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name

Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

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Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

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Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

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Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

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Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

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Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

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PNAS.0604919104

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

P1476

Epstein-Barr virus nuclear pro ...... nance of lymphoblastoid cells.

@en

P2093

Dai Iwakiri

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Kenzo Takada

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Satoko Ishikawa

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

Seiji Maruo

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Teru Kanda

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Yi Wu

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

P2860

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

A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4

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

Complete nucleotide sequence of the rhesus lymphocryptovirus: genetic validation for an Epstein-Barr virus animal model.

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

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

CDK inhibitors: positive and negative regulators of G1-phase progression

Physical and functional interactions between the corepressor CtBP and the Epstein-Barr virus nuclear antigen EBNA3C

BamHI E region of the Epstein-Barr virus genome encodes three transformation-associated nuclear proteins.

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19500-19505

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10.1073/PNAS.0604919104

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51

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103

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2006-12-11T00:00:00Z

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6640830

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17159137

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Epstein–Barr virus

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1748255

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