Extensive co-operation between the Epstein-Barr virus EBNA3 proteins in the manipulation of host gene expression and epigenetic chromatin modification.
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Role of EBNA-3 Family Proteins in EBV Associated B-cell LymphomagenesisThe EBNA3 family of Epstein-Barr virus nuclear proteins associates with the USP46/USP12 deubiquitination complexes to regulate lymphoblastoid cell line growthMolecular signature of Epstein Barr virus-positive Burkitt lymphoma and post-transplant lymphoproliferative disorder suggest different roles for Epstein Barr virus.Induction of p16(INK4a) is the major barrier to proliferation when Epstein-Barr virus (EBV) transforms primary B cells into lymphoblastoid cell lines.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.Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.Latent Epstein-Barr virus can inhibit apoptosis in B cells by blocking the induction of NOXA expressionE2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.Genome-wide DNA methylation as an epigenetic consequence of Epstein-Barr virus infection of immortalized keratinocytesEBV-positive diffuse large B-cell lymphoma of the elderlyThe effect of Epstein-Barr virus Latent Membrane Protein 2 expression on the kinetics of early B cell infectionModulation of enhancer looping and differential gene targeting by Epstein-Barr virus transcription factors directs cellular reprogramming.Inactivation of intergenic enhancers by EBNA3A initiates and maintains polycomb signatures across a chromatin domain encoding CXCL10 and CXCL9EBNA3C augments Pim-1 mediated phosphorylation and degradation of p21 to promote B-cell proliferationEpstein-Barr Virus Proteins EBNA3A and EBNA3C Together Induce Expression of the Oncogenic MicroRNA Cluster miR-221/miR-222 and Ablate Expression of Its Target p57KIP2.EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors.EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B CellsBIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBVEpstein-Barr virus-induced epigenetic alterations following transient infection.Epstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic SitesBiochemical and functional interactions of human papillomavirus proteins with polycomb group proteins.MYC activation and BCL2L11 silencing by a tumour virus through the large-scale reconfiguration of enhancer-promoter hubs.Epstein-Barr virus-associated B-cell lymphomas: pathogenesis and clinical outcomes.Burkitt lymphoma: the role of Epstein-Barr virus revisited.Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.EBV finds a polycomb-mediated, epigenetic solution to the problem of oncogenic stress responses triggered by infectionSwitching of EBV cycles between latent and lytic states.Epigenetic and transcriptional changes which follow Epstein-Barr virus infection of germinal center B cells and their relevance to the pathogenesis of Hodgkin's lymphoma.EBV Persistence--Introducing the Virus.EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.An essential EBV latent antigen 3C binds Bcl6 for targeted degradation and cell proliferation.Epigenetic Alterations in Epstein-Barr Virus-Associated Diseases.Core binding factor (CBF) is required for Epstein-Barr virus EBNA3 proteins to regulate target gene expressionRUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Combination of SAHA and bortezomib up-regulates CDKN2A and CDKN1A and induces apoptosis of Epstein-Barr virus-positive Wp-restricted Burkitt lymphoma and lymphoblastoid 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.Downregulation of integrin receptor-signaling genes by Epstein-Barr virus EBNA 3C via promoter-proximal and -distal binding elementsRoles of RUNX in B Cell Immortalisation.Oxidative stress enables Epstein-Barr virus-induced B-cell transformation by posttranscriptional regulation of viral and cellular growth-promoting factors.Early gene expression changes by Epstein-Barr virus infection of B-cells indicate CDKs and survivin as therapeutic targets for post-transplant lymphoproliferative diseases.
P2860
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P2860
Extensive co-operation between the Epstein-Barr virus EBNA3 proteins in the manipulation of host gene expression and epigenetic chromatin modification.
description
2010 nî lūn-bûn
@nan
2010 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Extensive co-operation between ...... enetic chromatin modification.
@ast
Extensive co-operation between ...... enetic chromatin modification.
@en
type
label
Extensive co-operation between ...... enetic chromatin modification.
@ast
Extensive co-operation between ...... enetic chromatin modification.
@en
prefLabel
Extensive co-operation between ...... enetic chromatin modification.
@ast
Extensive co-operation between ...... enetic chromatin modification.
@en
P2093
P2860
P50
P1433
P1476
Extensive co-operation between ...... enetic chromatin modification.
@en
P2093
Elisabeth Kremmer
Martin J Allday
P2860
P304
P356
10.1371/JOURNAL.PONE.0013979
P407
P577
2010-11-15T00:00:00Z