c-myc activation renders proliferation of Epstein-Barr virus (EBV)-transformed cells independent of EBV nuclear antigen 2 and latent membrane protein 1.
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An Epstein-Barr virus anti-apoptotic protein constitutively expressed in transformed cells and implicated in burkitt lymphomagenesis: the Wp/BHRF1 linkCoordinated regulation of iron-controlling genes, H-ferritin and IRP2, by c-MYCLatent membrane protein 1 of Epstein-Barr virus induces CD83 by the NF-kappaB signaling pathwayThe Role of Gammaherpesviruses in Cancer PathogenesisThe modulation of apoptosis by oncogenic virusesThe Epstein-Barr virus and its association with human cancers.Epstein-Barr virus nuclear antigen 2 (EBNA2) gene deletion is consistently linked with EBNA3A, -3B, and -3C expression in Burkitt's lymphoma cells and with increased resistance to apoptosis.MYC overexpression imposes a nonimmunogenic phenotype on Epstein-Barr virus-infected B cells.The expression and function of Epstein-Barr virus encoded latent genesEpstein-Barr virus and oncogenesis: from latent genes to tumours.EBNA3A association with RBP-Jkappa down-regulates c-myc and Epstein-Barr virus-transformed lymphoblast growth.Oncogenic DNA viruses.The role of Epstein-Barr virus in cancer.Burkitt's lymphoma: the Rosetta Stone deciphering Epstein-Barr virus biology.Viral carcinogenesis: factors inducing DNA damage and virus integrationElevation of c-MYC disrupts HLA class II-mediated immune recognition of human B cell tumorsThree restricted forms of Epstein-Barr virus latency counteracting apoptosis in c-myc-expressing Burkitt lymphoma cells.Apoptosis resistance, mitotic catastrophe, and loss of ploidy control in Burkitt lymphoma.EBNA2 interferes with the germinal center phenotype by downregulating BCL6 and TCL1 in non-Hodgkin's lymphoma cellsBurkitt lymphoma in the mouse.Identification of Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) target proteins by proteome analysis: activation of EBNA2 in conditionally immortalized B cells reflects early events after infection of primary B cells by EBV.Is the Epstein-Barr virus EBNA-1 protein an oncogen?c-Myc and Rel/NF-kappaB are the two master transcriptional systems activated in the latency III program of Epstein-Barr virus-immortalized B cells.Proof for EBV's sustaining role in Burkitt's lymphomas.Repression of the proapoptotic cellular BIK/NBK gene by Epstein-Barr virus antagonizes transforming growth factor β1-induced B-cell apoptosis.The Epstein-Barr virus and the pathogenesis of lymphoma.Epstein-Barr virus and Burkitt lymphoma.Reactivation of lytic replication from B cells latently infected with Epstein-Barr virus occurs with high S-phase cyclin-dependent kinase activity while inhibiting cellular DNA replication.EBV Persistence--Introducing the Virus.Epigenetic Alterations in Epstein-Barr Virus-Associated Diseases.Concurrent targeting of eicosanoid receptor 1/eicosanoid receptor 4 receptors and COX-2 induces synergistic apoptosis in Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus associated non-Hodgkin lymphoma cell lines.Different patterns of Epstein-Barr virus latency in endemic Burkitt lymphoma (BL) lead to distinct variants within the BL-associated gene expression signature.The proto-oncogene c-myc is a direct target gene of Epstein-Barr virus nuclear antigen 2.Human monocytic cell lines transformed in vitro by Epstein-Barr virus display a type II latency and LMP-1-dependent proliferation.c-Myc overexpression promotes a germinal center-like program in Burkitt's lymphoma.PNAEmu can significantly reduce Burkitt's lymphoma tumor burden in a SCID mice model: cells dissemination similar to the human disease.C-myc activation impairs the NF-kappaB and the interferon response: implications for the pathogenesis of Burkitt's lymphoma.Inhibition of Epstein-Barr virus (EBV) reactivation by short interfering RNAs targeting p38 mitogen-activated protein kinase or c-myc in EBV-positive epithelial cells.Regulation of Epstein-Barr virus latency type by the chromatin boundary factor CTCF.Epstein-Barr virus-associated Burkitt lymphomagenesis selects for downregulation of the nuclear antigen EBNA2.
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c-myc activation renders proliferation of Epstein-Barr virus (EBV)-transformed cells independent of EBV nuclear antigen 2 and latent membrane protein 1.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on September 1996
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
c-myc activation renders proli ...... and latent membrane protein 1.
@en
c-myc activation renders proliferation of Epstein-Barr virus
@nl
type
label
c-myc activation renders proli ...... and latent membrane protein 1.
@en
c-myc activation renders proliferation of Epstein-Barr virus
@nl
prefLabel
c-myc activation renders proli ...... and latent membrane protein 1.
@en
c-myc activation renders proliferation of Epstein-Barr virus
@nl
P2093
P2860
P356
P1476
c-myc activation renders proli ...... and latent membrane protein 1.
@en
P2093
Bornkamm GW
Christoph B
Geltinger C
Hörtnagel K
P2860
P304
10411-10416
P356
10.1073/PNAS.93.19.10411
P407
P577
1996-09-01T00:00:00Z