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Article: Role of defective Oct-2 and OCA-B expression in immunoglobulin production and Kaposi's sarcoma-associated herpesvirus lytic reactivation in primary effusion lymphoma

TitleRole of defective Oct-2 and OCA-B expression in immunoglobulin production and Kaposi's sarcoma-associated herpesvirus lytic reactivation in primary effusion lymphoma
Authors
Issue Date2009
Citation
Journal of Virology, 2009, v. 83, n. 9, p. 4308-4315 How to Cite?
AbstractPrimary effusion lymphoma (PEL) is a distinct type of B-cell non-Hodgkin lymphoma characterized by the presence of Kaposi's sarcoma-associated herpesvirus (KSHV/human herpesvirus 8). Despite having a genotype and gene expression signature of highly differentiated B cells, PEL does not usually express surface or cytoplasmic immunoglobulin (Ig). We show the lack of Oct-2 and OCA-B transcription factors to be responsible, at least in part, for this defect in Ig production. Like Ig genes, ORF50, the key regulator of the switch from latency to lytic reactivation, contains an octamer motif within its promoter. We therefore examined the impact of Oct-2 and OCA-B on ORF50 activation. The binding of Oct-1 to the ORF50 promoter has been shown to significantly enhance ORF50 transactivation. We found that Oct-2, on the other hand, inhibited ORF50 expression and consequently lytic reactivation by competing with Oct-1 for the octamer motif in the ORF50 promoter. Our data suggest that Oct-2 downregulation in infected cells would be favorable to KSHV in allowing for efficient viral reactivation. Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/285652
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDi Bartolo, Daniel L.-
dc.contributor.authorHyjek, Elizabeth-
dc.contributor.authorKeller, Shannon-
dc.contributor.authorGuasparri, Ilaria-
dc.contributor.authorDeng, Hongyu-
dc.contributor.authorSun, Ren-
dc.contributor.authorChadburn, Amy-
dc.contributor.authorKnowles, Daniel M.-
dc.contributor.authorCesarman, Ethel-
dc.date.accessioned2020-08-18T04:56:18Z-
dc.date.available2020-08-18T04:56:18Z-
dc.date.issued2009-
dc.identifier.citationJournal of Virology, 2009, v. 83, n. 9, p. 4308-4315-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285652-
dc.description.abstractPrimary effusion lymphoma (PEL) is a distinct type of B-cell non-Hodgkin lymphoma characterized by the presence of Kaposi's sarcoma-associated herpesvirus (KSHV/human herpesvirus 8). Despite having a genotype and gene expression signature of highly differentiated B cells, PEL does not usually express surface or cytoplasmic immunoglobulin (Ig). We show the lack of Oct-2 and OCA-B transcription factors to be responsible, at least in part, for this defect in Ig production. Like Ig genes, ORF50, the key regulator of the switch from latency to lytic reactivation, contains an octamer motif within its promoter. We therefore examined the impact of Oct-2 and OCA-B on ORF50 activation. The binding of Oct-1 to the ORF50 promoter has been shown to significantly enhance ORF50 transactivation. We found that Oct-2, on the other hand, inhibited ORF50 expression and consequently lytic reactivation by competing with Oct-1 for the octamer motif in the ORF50 promoter. Our data suggest that Oct-2 downregulation in infected cells would be favorable to KSHV in allowing for efficient viral reactivation. Copyright © 2009, American Society for Microbiology. All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleRole of defective Oct-2 and OCA-B expression in immunoglobulin production and Kaposi's sarcoma-associated herpesvirus lytic reactivation in primary effusion lymphoma-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.02196-08-
dc.identifier.pmid19224997-
dc.identifier.pmcidPMC2668464-
dc.identifier.scopuseid_2-s2.0-66149139159-
dc.identifier.volume83-
dc.identifier.issue9-
dc.identifier.spage4308-
dc.identifier.epage4315-
dc.identifier.isiWOS:000265041600030-
dc.identifier.issnl0022-538X-

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