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Article: Myc is required for the maintenance of Kaposi's sarcoma-associated herpesvirus latency

TitleMyc is required for the maintenance of Kaposi's sarcoma-associated herpesvirus latency
Authors
Issue Date2010
Citation
Journal of Virology, 2010, v. 84, n. 17, p. 8945-8948 How to Cite?
AbstractMyc is deregulated by Kaposi's sarcoma-associated herpesvirus (KSHV) latent proteins, but its role in KSHV latency is not clear. We found that Myc knockdown with RNA interference (RNAi) induced KSHV reactivation and increased the protein and mRNA levels of RTA, a key viral regulator of KSHV reactivation. Myc knockdown increased, whereas Myc overexpression inhibited, RTA promoter activity. KSHV reactivation and the activation of the RTA promoter induced by Myc depletion were inhibited by c-Jun N-terminal kinase (JNK) and p38 inhibitors but not by a MEK1 inhibitor. Myc knockdown inhibited primary effusion lymphoma (PEL) cell proliferation through inducing apoptosis and G1 cell cycle arrest. Thus, Myc may be a key cellular node coupling cellular transformation and KSHV latency. Copyright © 2010, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/285671
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, Xudong-
dc.contributor.authorChen, Shijia-
dc.contributor.authorFeng, Jun-
dc.contributor.authorDeng, Hongyu-
dc.contributor.authorSun, Ren-
dc.date.accessioned2020-08-18T04:56:21Z-
dc.date.available2020-08-18T04:56:21Z-
dc.date.issued2010-
dc.identifier.citationJournal of Virology, 2010, v. 84, n. 17, p. 8945-8948-
dc.identifier.issn0022-538X-
dc.identifier.urihttp://hdl.handle.net/10722/285671-
dc.description.abstractMyc is deregulated by Kaposi's sarcoma-associated herpesvirus (KSHV) latent proteins, but its role in KSHV latency is not clear. We found that Myc knockdown with RNA interference (RNAi) induced KSHV reactivation and increased the protein and mRNA levels of RTA, a key viral regulator of KSHV reactivation. Myc knockdown increased, whereas Myc overexpression inhibited, RTA promoter activity. KSHV reactivation and the activation of the RTA promoter induced by Myc depletion were inhibited by c-Jun N-terminal kinase (JNK) and p38 inhibitors but not by a MEK1 inhibitor. Myc knockdown inhibited primary effusion lymphoma (PEL) cell proliferation through inducing apoptosis and G1 cell cycle arrest. Thus, Myc may be a key cellular node coupling cellular transformation and KSHV latency. Copyright © 2010, American Society for Microbiology. All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofJournal of Virology-
dc.titleMyc is required for the maintenance of Kaposi's sarcoma-associated herpesvirus latency-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/JVI.00244-10-
dc.identifier.pmid20573831-
dc.identifier.pmcidPMC2919007-
dc.identifier.scopuseid_2-s2.0-77956634358-
dc.identifier.volume84-
dc.identifier.issue17-
dc.identifier.spage8945-
dc.identifier.epage8948-
dc.identifier.eissn1098-5514-
dc.identifier.isiWOS:000280605300052-
dc.identifier.issnl0022-538X-

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