Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.
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Role 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 growthEpstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infectionEpstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1Epstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.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 CXCL9Epstein-Barr virus-positive T/NK-cell lymphoproliferative disordersLMP1-deficient Epstein-Barr virus mutant requires T cells for lymphomagenesis.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.EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B CellsEpstein-Barr virus oncoprotein super-enhancers control B cell growthMetabolic stress is a barrier to Epstein-Barr virus-mediated B-cell immortalization.Epstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic SitesBiochemical and functional interactions of human papillomavirus proteins with polycomb group proteins.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 proliferationEBV finds a polycomb-mediated, epigenetic solution to the problem of oncogenic stress responses triggered by infectionModes of infection and oncogenesis by the Epstein-Barr virus.Role of epigenetics in EBV regulation and pathogenesis.Epstein-Barr virus latency: current and future perspectives.EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.Core binding factor (CBF) is required for Epstein-Barr virus EBNA3 proteins to regulate target gene expressionEpstein-Barr virus nuclear protein EBNA3C directly induces expression of AID and somatic mutations in B cells.Latent Membrane Protein 1 (LMP1) and LMP2A Collaborate To Promote Epstein-Barr Virus-Induced B Cell Lymphomas in a Cord Blood-Humanized Mouse Model but Are Not Essential.Mitogen-induced B-cell proliferation activates Chk2-dependent G1/S cell cycle arrestThe Epstein-Barr Virus Regulome in Lymphoblastoid Cells.EBV and Apoptosis: The Viral Master Regulator of Cell Fate?Epstein-Barr Virus (EBV) Latent Protein EBNA3A Directly Targets and Silences the STK39 Gene in B Cells Infected by EBV.Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome.Differential DNA methylation profiles of human B lymphocytes and Epstein-Barr virus-immortalized B lymphocytes.EBV persistence without its EBNA3A and 3C oncogenes in vivo.The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.An EBNA3C-deleted Epstein-Barr virus (EBV) mutant causes B-cell lymphomas with delayed onset in a cord blood-humanized mouse modelEpstein-Barr Virus Nuclear Antigen 3C Inhibits Expression of and the Locus via Interaction with the Histone Lysine Demethylase KDM2BEpstein-Barr Virus-Associated Malignancies: Roles of Viral Oncoproteins in Carcinogenesis
P2860
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P2860
Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.
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2013 nî lūn-bûn
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2013 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2013年の論文
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2013年論文
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2013年論文
@zh-hant
2013年論文
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2013年論文
@zh-mo
2013年論文
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2013年论文
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name
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@ast
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@en
type
label
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@ast
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@en
prefLabel
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@ast
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@en
P2093
P2860
P50
P1433
P1476
Induction of p16(INK4a) is the ...... nto lymphoblastoid cell lines.
@en
P2093
Gillian A Parker
Lenka Skalska
Martin J Allday
P2860
P304
P356
10.1371/JOURNAL.PPAT.1003187
P577
2013-02-21T00:00:00Z