EBNA-2 and EBNA-3C extensively and mutually exclusively associate with RBPJkappa in Epstein-Barr virus-transformed B lymphocytes.
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CIR, a corepressor linking the DNA binding factor CBF1 to the histone deacetylase complexNF-kappa B inhibition causes spontaneous apoptosis in Epstein-Barr virus-transformed lymphoblastoid cellsEpstein-Barr virus encoded nuclear protein EBNA-3 binds a novel human uridine kinase/uracil phosphoribosyltransferaseA role for SKIP in EBNA2 activation of CBF1-repressed promotersEpstein-Barr virus BamHi-a rightward transcript-encoded RPMS protein interacts with the CBF1-associated corepressor CIR to negatively regulate the activity of EBNA2 and NotchICEpstein-Barr virus immortalization: Notch2 interacts with CBF1 and blocks differentiationThe Role of Gammaherpesviruses in Cancer PathogenesisModulation of histone acetyltransferase activity through interaction of epstein-barr nuclear antigen 3C with prothymosin alphaThe EBNA3 family of Epstein-Barr virus nuclear proteins associates with the USP46/USP12 deubiquitination complexes to regulate lymphoblastoid cell line growthResidues 231 to 280 of the Epstein-Barr virus nuclear protein 2 are not essential for primary B-lymphocyte growth transformation.The latency-associated nuclear antigen encoded by Kaposi's sarcoma-associated herpesvirus activates two major essential Epstein-Barr virus latent promotersEpstein-Barr virus nuclear protein 3A domains essential for growth of lymphoblasts: transcriptional regulation through RBP-Jkappa/CBF1 is critical.Viral latency and its regulation: lessons from the gamma-herpesviruses.Epstein-Barr virus nuclear antigen 3C stabilizes Gemin3 to block p53-mediated apoptosis.E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.Molecular virology of Epstein-Barr virus.Epstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.Epstein-barr virus-induced changes in B-lymphocyte gene expression.Complete genomic sequence of an Epstein-Barr virus-related herpesvirus naturally infecting a new world primate: a defining point in the evolution of oncogenic lymphocryptoviruses.EBNA3A association with RBP-Jkappa down-regulates c-myc and Epstein-Barr virus-transformed lymphoblast growth.Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.EBNA3C attenuates the function of p53 through interaction with inhibitor of growth family proteins 4 and 5Epstein-Barr virus nuclear antigen 3C targets p53 and modulates its transcriptional and apoptotic activities.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.Three restricted forms of Epstein-Barr virus latency counteracting apoptosis in c-myc-expressing Burkitt lymphoma cells.Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells.EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B CellsEpstein-Barr virus nuclear protein LP stimulates EBNA-2 acidic domain-mediated transcriptional activationEBV 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 growthEpstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic SitesRole of NF-kappa B in cell survival and transcription of latent membrane protein 1-expressing or Epstein-Barr virus latency III-infected cells.Epstein-Barr virus nuclear protein EBNA3C residues critical for maintaining lymphoblastoid cell growth.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.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.At a crossroads: human DNA tumor viruses and the host DNA damage response.RUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Epstein-Barr virus EBNA-3C is targeted to and regulates expression from the bidirectional LMP-1/2B promoter.
P2860
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P2860
EBNA-2 and EBNA-3C extensively and mutually exclusively associate with RBPJkappa in Epstein-Barr virus-transformed B lymphocytes.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
1996年论文
@zh
1996年论文
@zh-cn
name
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@ast
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@en
type
label
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@ast
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@en
prefLabel
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@ast
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@en
P2093
P2860
P1433
P1476
EBNA-2 and EBNA-3C extensively ...... rus-transformed B lymphocytes.
@en
P2093
C L Miller
E Johannsen
S R Grossman
P2860
P304
P407
P577
1996-06-01T00:00:00Z