Epstein-Barr virus nuclear protein EBNA3C residues critical for maintaining lymphoblastoid cell growth.
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The Modulation of Apoptotic Pathways by GammaherpesvirusesRole of EBNA-3 Family Proteins in EBV Associated B-cell LymphomagenesisEpigenetic Impact on EBV Associated B-Cell LymphomagenesisEpstein-Barr virus latent genesThe EBNA3 family of Epstein-Barr virus nuclear proteins associates with the USP46/USP12 deubiquitination complexes to regulate lymphoblastoid cell line growthEpigenetic repression of p16(INK4A) by latent Epstein-Barr virus requires the interaction of EBNA3A and EBNA3C with CtBP.Epstein-Barr virus nuclear antigen 3C facilitates G1-S transition by stabilizing and enhancing the function of cyclin D1.E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.Genomic diversity of Epstein-Barr virus genomes isolated from primary nasopharyngeal carcinoma biopsy samples.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.The EBV Latent Antigen 3C Inhibits Apoptosis through Targeted Regulation of Interferon Regulatory Factors 4 and 8.EBNA3C attenuates the function of p53 through interaction with inhibitor of growth family proteins 4 and 5Epstein-Barr virus nuclear antigen 3A partially coincides with EBNA3C genome-wide and is tethered to DNA through BATF complexes.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.EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B CellsEpstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic SitesEpstein-Barr virus nuclear protein 3C domains necessary for lymphoblastoid cell growth: interaction with RBP-Jkappa regulates TCL1.Epstein-Barr virus nuclear antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.Epstein-Barr virus-associated B-cell lymphomas: pathogenesis and clinical outcomes.Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Dissecting the contribution of EBNA3C domains important for EBV-induced B-cell growth and proliferation.An EBV recombinant deleted for residues 130-159 in EBNA3C can deregulate p53/Mdm2 and Cyclin D1/CDK6 which results in apoptosis and reduced cell proliferation.RUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Epstein-Barr virus essential antigen EBNA3C attenuates H2AX expression.EBNA3C regulates p53 through induction of Aurora kinase B.EBNA3C interacts with Gadd34 and counteracts the unfolded protein response.The Epstein-Barr Virus Regulome in Lymphoblastoid Cells.The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression of and the Locus via Interaction with the Histone Lysine Demethylase KDM2B
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Epstein-Barr virus nuclear protein EBNA3C residues critical for maintaining lymphoblastoid cell growth.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 23 February 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
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Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
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type
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Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
@en
Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
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Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
@en
Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
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P2093
P2860
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P1476
Epstein-Barr virus nuclear pro ...... ng lymphoblastoid cell growth.
@en
P2093
Elliott D Kieff
Kenzo Takada
Seiji Maruo
Teru Kanda
P2860
P304
P356
10.1073/PNAS.0813134106
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P577
2009-02-23T00:00:00Z