EBNA-2 and EBNA-LP cooperate to cause G0 to G1 transition during immortalization of resting human B lymphocytes by Epstein-Barr virus.
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Epstein-Barr virus nuclear antigen 3C interacts with and enhances the stability of the c-Myc oncoproteinHerpes simplex virus 1 alpha regulatory protein ICP0 interacts with and stabilizes the cell cycle regulator cyclin D3A role for SKIP in EBNA2 activation of CBF1-repressed promotersCAK-independent activation of CDK6 by a viral cyclinEpstein-Barr virus immortalization: Notch2 interacts with CBF1 and blocks differentiationEBNA2 and activated Notch induce expression of BATFEpstein-Barr virus provides a new paradigm: a requirement for the immediate inhibition of apoptosis.Protein kinase A associates with HA95 and affects transcriptional coactivation by Epstein-Barr virus nuclear proteins.PRIMA-1MET induces nucleolar translocation of Epstein-Barr virus-encoded EBNA-5 protein.Interaction of Epstein-Barr virus nuclear antigen leader protein (EBNA-LP) with HS1-associated protein X-1: implication of cytoplasmic function of EBNA-LP.BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2.Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.CD34+ cord blood cell-transplanted Rag2-/- gamma(c)-/- mice as a model for Epstein-Barr virus infectionCharacterization and cell cycle regulation of the major Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) latent genes and their promoter.The Epstein-Barr virus promoter initiating B-cell transformation is activated by RFX proteins and the B-cell-specific activator protein BSAP/Pax5Interferon regulatory factor 7 is induced by Epstein-Barr virus latent membrane protein 1Sequence and functional analysis of EBNA-LP and EBNA2 proteins from nonhuman primate lymphocryptovirusesE2F proteins are posttranslationally modified concomitantly with a reduction in nuclear binding activity in cells infected with herpes simplex virus 1.Control of cell cycle entry and apoptosis in B lymphocytes infected by Epstein-Barr virus.Signaling activities of gammaherpesvirus membrane proteinsGenetic dissection of cell growth arrest functions mediated by the Epstein-Barr virus lytic gene product, ZtaEpstein-Barr virus nuclear antigen 3C facilitates G1-S transition by stabilizing and enhancing the function of cyclin D1.Activated Notch1 can transiently substitute for EBNA2 in the maintenance of proliferation of LMP1-expressing immortalized B cells.EBNA-LP associates with cellular proteins including DNA-PK and HA95.Direct and indirect regulation of cytokine and cell cycle proteins by EBNA-2 during Epstein-Barr virus infection.Identification of major phosphorylation sites of Epstein-Barr virus nuclear antigen leader protein (EBNA-LP): ability of EBNA-LP to induce latent membrane protein 1 cooperatively with EBNA-2 is regulated by phosphorylationThe Epstein-Barr virus and its association with human cancers.Interferon regulatory factor 2 represses the Epstein-Barr virus BamHI Q latency promoter in type III latency.Host factors LR1 and Sp1 regulate the Fp promoter of Epstein-Barr virus.C-terminal region of EBNA-2 determines the superior transforming ability of type 1 Epstein-Barr virus by enhanced gene regulation of LMP-1 and CXCR7.Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.Evolutionary aspects of oncogenic herpesvirusesThe expression and function of Epstein-Barr virus encoded latent genesUpregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.Epstein-Barr virus EBNA2 blocks Nur77- mediated apoptosisBurkitt lymphoma: pathogenesis and immune evasion.Molecular virology of Epstein-Barr virus.Herpes simplex virus 1 mutant in which the ICP0 HUL-1 E3 ubiquitin ligase site is disrupted stabilizes cdc34 but degrades D-type cyclins and exhibits diminished neurotoxicityEpstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.Strategies in subversion: de-regulation of the mammalian cell cycle by viral gene products.
P2860
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P2860
EBNA-2 and EBNA-LP cooperate to cause G0 to G1 transition during immortalization of resting human B lymphocytes by Epstein-Barr virus.
description
1994 nî lūn-bûn
@nan
1994年の論文
@ja
1994年学术文章
@wuu
1994年学术文章
@zh-cn
1994年学术文章
@zh-hans
1994年学术文章
@zh-my
1994年学术文章
@zh-sg
1994年學術文章
@yue
1994年學術文章
@zh
1994年學術文章
@zh-hant
name
EBNA-2 and EBNA-LP cooperate t ...... hocytes by Epstein-Barr virus.
@en
type
label
EBNA-2 and EBNA-LP cooperate t ...... hocytes by Epstein-Barr virus.
@en
prefLabel
EBNA-2 and EBNA-LP cooperate t ...... hocytes by Epstein-Barr virus.
@en
P2093
P2860
P1433
P1476
EBNA-2 and EBNA-LP cooperate t ...... phocytes by Epstein-Barr virus
@en
P2093
P2860
P304
P356
10.1002/J.1460-2075.1994.TB06634.X
P407
P577
1994-07-01T00:00:00Z