The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
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Epstein-Barr virus nuclear antigen 3C putative repression domain mediates coactivation of the LMP1 promoter with EBNA-2.Epstein-Barr virus BHRF1 micro- and stable RNAs during latency III and after induction of replicationEBNA2 and activated Notch induce expression of BATFLatent membrane protein 1 of Epstein-Barr virus induces CD83 by the NF-kappaB signaling pathwayRole of EBNA-3 Family Proteins in EBV Associated B-cell LymphomagenesisThe Role of Gammaherpesviruses in Cancer PathogenesisEpstein-Barr Virus: Diseases Linked to Infection and TransformationProtein kinase A associates with HA95 and affects transcriptional coactivation by Epstein-Barr virus nuclear proteins.Binding of the heterogeneous ribonucleoprotein K (hnRNP K) to the Epstein-Barr virus nuclear antigen 2 (EBNA2) enhances viral LMP2A expressionEpstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene BimEBNA1 regulates cellular gene expression by binding cellular promotersInduction of ectopic Myc target gene JAG2 augments hypoxic growth and tumorigenesis in a human B-cell model.Hyperphosphorylation of EBNA2 by Epstein-Barr virus protein kinase suppresses transactivation of the LMP1 promoter.c-Myc dysregulation is a co-transforming event for nuclear factor-κB activated B cells.Notch1IC partially replaces EBNA2 function in B cells immortalized by Epstein-Barr virus.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.Epstein-Barr virus nuclear protein 2 has at least two N-terminal domains that mediate self-associationDirect and indirect regulation of cytokine and cell cycle proteins by EBNA-2 during Epstein-Barr virus infection.Correlation of Epstein-Barr virus and its encoded proteins with Helicobacter pylori and expression of c-met and c-myc in gastric carcinomaA somatic knockout of CBF1 in a human B-cell line reveals that induction of CD21 and CCR7 by EBNA-2 is strictly CBF1 dependent and that downregulation of immunoglobulin M is partially CBF1 independent.Epstein-Barr virus nuclear protein 3A domains essential for growth of lymphoblasts: transcriptional regulation through RBP-Jkappa/CBF1 is critical.The nuclear chaperone nucleophosmin escorts an Epstein-Barr Virus nuclear antigen to establish transcriptional cascades for latent infection in human B cellsDevelopments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.The expression and function of Epstein-Barr virus encoded latent genesBurkitt lymphoma: pathogenesis and immune evasion.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.The EBNA2 polyproline region is dispensable for Epstein-Barr virus-mediated immortalization maintenanceEpstein-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.RNAs induced by Epstein-Barr virus nuclear antigen 2 in lymphoblastoid cell lines.Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cellsEpstein-Barr virus activates beta-catenin in type III latently infected B lymphocyte lines: association with deubiquitinating enzymesModulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming.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.Cellular target genes of Epstein-Barr virus nuclear antigen 2.Epstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell growth.
P2860
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P2860
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
@en
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
@nl
type
label
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
@en
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
@nl
prefLabel
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
@en
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.
@nl
P2093
P2860
P1433
P1476
The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2
@en
P2093
P2860
P304
P407
P577
1999-05-01T00:00:00Z