Epstein-Barr virus nuclear antigen 3C putative repression domain mediates coactivation of the LMP1 promoter with EBNA-2.
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Epstein-Barr virus latent membrane protein 1 (LMP1) C-terminal-activating region 3 contributes to LMP1-mediated cellular migration via its interaction with Ubc9NXP-2 association with SUMO-2 depends on lysines required for transcriptional repressionInterferon regulatory factor 7 regulates expression of Epstein-Barr virus latent membrane protein 1: a regulatory circuitThe Modulation of Apoptotic Pathways by GammaherpesvirusesEpstein-Barr virus latent genesThe EBNA3 family of Epstein-Barr virus nuclear proteins associates with the USP46/USP12 deubiquitination complexes to regulate lymphoblastoid cell line growthModulation of Epstein-Barr virus nuclear antigen 2-dependent transcription by protein arginine methyltransferase 5.Epstein-Barr virus nuclear protein 3A domains essential for growth of lymphoblasts: transcriptional regulation through RBP-Jkappa/CBF1 is critical.Interferon regulatory factor 5 represses expression of the Epstein-Barr virus oncoprotein LMP1: braking of the IRF7/LMP1 regulatory circuit.Epstein-Barr virus nuclear antigen 3A protein regulates CDKN2B transcription via interaction with MIZ-1Epstein-barr virus-induced changes in B-lymphocyte gene expression.EBNA3A association with RBP-Jkappa down-regulates c-myc and Epstein-Barr virus-transformed lymphoblast growth.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.EBNA3C coactivation with EBNA2 requires a SUMO homology domain.Functional modulation of the metastatic suppressor Nm23-H1 by oncogenic virusesEpstein-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 nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells.Direct interactions between Epstein-Barr virus leader protein LP and the EBNA2 acidic domain underlie coordinate transcriptional regulation.The ATM/ATR signaling effector Chk2 is targeted by Epstein-Barr virus nuclear antigen 3C to release the G2/M cell cycle blockLMP1-Induced Sumoylation Influences the Maintenance of Epstein-Barr Virus Latency through KAP1EBV Nuclear Antigen 3C Mediates Regulation of E2F6 to Inhibit E2F1 Transcription and Promote Cell Proliferation.Epstein-Barr Virus nuclear protein EBNA3A is critical for maintaining lymphoblastoid cell line growthEBV-encoded EBNA-6 binds and targets MRS18-2 to the nucleus, resulting in the disruption of pRb-E2F1 complexesRibosome Protein L4 is essential for Epstein-Barr Virus Nuclear Antigen 1 functionMolecular approaches towards characterization, monitoring and targeting of viral-associated hematological malignancies.Induction of Epstein-Barr Virus Oncoprotein LMP1 by Transcription Factors AP-2 and Early B Cell FactorMitosis-specific hyperphosphorylation of Epstein-Barr virus nuclear antigen 2 suppresses its function.Epstein-Barr virus nuclear protein EBNA3C residues critical for maintaining lymphoblastoid cell growth.Epstein-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.Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Dynamic Epstein-Barr virus gene expression on the path to B-cell transformation.EBNA-3B- and EBNA-3C-regulated cellular genes in Epstein-Barr virus-immortalized lymphoblastoid cell lines.Deregulation of the cell cycle machinery by Epstein-Barr virus nuclear antigen 3C.At a crossroads: human DNA tumor viruses and the host DNA damage response.Epstein-Barr virus EBNA-3C is targeted to and regulates expression from the bidirectional LMP-1/2B promoter.A positive autoregulatory loop of LMP1 expression and STAT activation in epithelial cells latently infected with Epstein-Barr virus.EBNA3C interacts with Gadd34 and counteracts the unfolded protein response.Epstein-Barr virus nuclear antigen 3C augments Mdm2-mediated p53 ubiquitination and degradation by deubiquitinating Mdm2.
P2860
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P2860
Epstein-Barr virus nuclear antigen 3C putative repression domain mediates coactivation of the LMP1 promoter with EBNA-2.
description
2002 nî lūn-bûn
@nan
2002 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2
@nl
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@ast
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@en
type
label
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2
@nl
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@ast
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@en
prefLabel
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2
@nl
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@ast
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@en
P2860
P3181
P1433
P1476
Epstein-Barr virus nuclear ant ...... the LMP1 promoter with EBNA-2.
@en
P2093
Eric Johannsen
Jeffrey Lin
P2860
P304
P3181
P356
10.1128/JVI.76.1.232-242.2002
P407
P577
2002-01-01T00:00:00Z