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Article: Lytic replication-associated protein (RAP) encoded by Kaposi sarcoma-associated herpesvirus causes p21CIP-1-mediated G1 cell cycle arrest through CCAAT/enhancer-binding protein-α

TitleLytic replication-associated protein (RAP) encoded by Kaposi sarcoma-associated herpesvirus causes p21CIP-1-mediated G1 cell cycle arrest through CCAAT/enhancer-binding protein-α
Authors
Issue Date2002
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2002, v. 99 n. 16, p. 10683-10688 How to Cite?
AbstractKaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic DNA virus that causes Kaposi sarcoma and AIDS-related primary effusion lymphoma (PEL). Here we show that KSHV lytic cycle replication in PEL cells induces G1 cell cycle arrest, presumably to facilitate the progression of viral DNA replication. Expression of a KSHV-encoded early lytic protein referred to as RAP or K8 is induced within 12-24 h after the onset of lytic cycle induction in host PEL cells, and coincides with increased levels of both the endogenous C/EBPα and p21CIP-1 proteins in the nucleus of the same cells. The KSHV RAP protein binds to C/EBPα in vitro and stimulates C/EBPα-induced expression from both the C/EBPα and p21 promoters in cotransfected cells. A recombinant adenovirus expressing the RAP protein induced the expression of both the C/EBPα and p21 proteins in primary human fibroblasts, and flow cytometric analysis revealed a dramatic inhibition of G1 to S cell cycle progression in the same cells. All of these effects were abolished in cells that lack C/EBPα or by deletion of the basic/leucine zipper region in RAP that interacts with C/EBPα. Therefore, C/EBPα is essential for the p21-mediated inhibition of G1 to S-phase progression by RAP in KSHV-infected host cells.
Persistent Identifierhttp://hdl.handle.net/10722/157341
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWu, FYen_US
dc.contributor.authorTang, QQen_US
dc.contributor.authorChen, Hen_US
dc.contributor.authorAprhys, Cen_US
dc.contributor.authorFarrell, Cen_US
dc.contributor.authorChen, Jen_US
dc.contributor.authorFujimuro, Men_US
dc.contributor.authorLane, MDen_US
dc.contributor.authorHayward, GSen_US
dc.date.accessioned2012-08-08T08:49:03Z-
dc.date.available2012-08-08T08:49:03Z-
dc.date.issued2002en_US
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2002, v. 99 n. 16, p. 10683-10688en_US
dc.identifier.issn0027-8424en_US
dc.identifier.urihttp://hdl.handle.net/10722/157341-
dc.description.abstractKaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic DNA virus that causes Kaposi sarcoma and AIDS-related primary effusion lymphoma (PEL). Here we show that KSHV lytic cycle replication in PEL cells induces G1 cell cycle arrest, presumably to facilitate the progression of viral DNA replication. Expression of a KSHV-encoded early lytic protein referred to as RAP or K8 is induced within 12-24 h after the onset of lytic cycle induction in host PEL cells, and coincides with increased levels of both the endogenous C/EBPα and p21CIP-1 proteins in the nucleus of the same cells. The KSHV RAP protein binds to C/EBPα in vitro and stimulates C/EBPα-induced expression from both the C/EBPα and p21 promoters in cotransfected cells. A recombinant adenovirus expressing the RAP protein induced the expression of both the C/EBPα and p21 proteins in primary human fibroblasts, and flow cytometric analysis revealed a dramatic inhibition of G1 to S cell cycle progression in the same cells. All of these effects were abolished in cells that lack C/EBPα or by deletion of the basic/leucine zipper region in RAP that interacts with C/EBPα. Therefore, C/EBPα is essential for the p21-mediated inhibition of G1 to S-phase progression by RAP in KSHV-infected host cells.en_US
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_US
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.subject.mesh3T3 Cellsen_US
dc.subject.meshAdenoviruses, Humanen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBasic-Leucine Zipper Transcription Factorsen_US
dc.subject.meshCcaat-Enhancer-Binding Protein-Alpha - Genetics - Metabolismen_US
dc.subject.meshCarrier Proteins - Genetics - Metabolismen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshCell Line, Transformeden_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P21en_US
dc.subject.meshCyclins - Genetics - Metabolismen_US
dc.subject.meshFibroblasts - Cytologyen_US
dc.subject.meshG1 Phaseen_US
dc.subject.meshGenetic Vectorsen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHerpesvirus 8, Human - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLeucine Zippersen_US
dc.subject.meshMiceen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshS Phaseen_US
dc.subject.meshSarcoma, Kaposi - Virologyen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshViral Proteins - Genetics - Metabolismen_US
dc.titleLytic replication-associated protein (RAP) encoded by Kaposi sarcoma-associated herpesvirus causes p21CIP-1-mediated G1 cell cycle arrest through CCAAT/enhancer-binding protein-αen_US
dc.typeArticleen_US
dc.identifier.emailChen, H:hlchen@hkucc.hku.hken_US
dc.identifier.authorityChen, H=rp00383en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1073/pnas.162352299en_US
dc.identifier.pmid12145325-
dc.identifier.scopuseid_2-s2.0-0036677565en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036677565&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume99en_US
dc.identifier.issue16en_US
dc.identifier.spage10683en_US
dc.identifier.epage10688en_US
dc.identifier.isiWOS:000177343200084-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWu, FY=36991458700en_US
dc.identifier.scopusauthoridTang, QQ=7201631934en_US
dc.identifier.scopusauthoridChen, H=26643315400en_US
dc.identifier.scopusauthoridApRhys, C=6506181422en_US
dc.identifier.scopusauthoridFarrell, C=7102327845en_US
dc.identifier.scopusauthoridChen, J=7501878756en_US
dc.identifier.scopusauthoridFujimuro, M=6603781101en_US
dc.identifier.scopusauthoridLane, MD=7401977437en_US
dc.identifier.scopusauthoridHayward, GS=7101602499en_US
dc.identifier.issnl0027-8424-

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