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Article: Human immunodeficiency virus type 1 replication and regulation of APOBEC3G by peptidyl prolyl isomerase Pin1

TitleHuman immunodeficiency virus type 1 replication and regulation of APOBEC3G by peptidyl prolyl isomerase Pin1
Authors
Issue Date2008
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/
Citation
Journal Of Virology, 2008, v. 82 n. 20, p. 9928-9936 How to Cite?
AbstractAPOBEC3G (A3G) is a cytidine deaminase that restricts human immunodeficiency virus type 1 (HIV-1) replication. HIV-1 synthesizes a viral infectivity factor (Vif) to counter A3G restriction. Currently, it is poorly understood how A3G expression/activity is regulated by cellular factors. Here, we show that the prolyl isomerase Pin1 protein modulates A3G expression. Pin1 was found to be an A3G-interacting protein that reduces A3G expression and its incorporation into HIV-1 virion, thereby limiting A3G-mediated restriction of HIV-1. Intriguingly, HIV-1 infection modulates the phosphorylation state of Pin1, enhancing its ability to moderate A3G activity. These new findings suggest a potential Vif-independent way for HIV-1 to moderate the cellular action of A3G.
Persistent Identifierhttp://hdl.handle.net/10722/152577
ISSN
2015 Impact Factor: 4.606
2015 SCImago Journal Rankings: 3.347
ISI Accession Number ID
Funding AgencyGrant Number
NIAID
NIH
Intramural AIDS Targeted Antiviral Program (IATAP)
Funding Information:

We are grateful to Alicia Buckler-White and Ronald Plishka for sequence analysis. We also thank the members of K.-T.J.' s laboratory for critical readings of the manuscript.

 

DC FieldValueLanguage
dc.contributor.authorWatashi, Ken_US
dc.contributor.authorKhan, Men_US
dc.contributor.authorYedavalli, VRKen_US
dc.contributor.authorYeung, MLen_US
dc.contributor.authorStrebe, Ken_US
dc.contributor.authorJeang, KTen_US
dc.date.accessioned2012-07-12T01:51:57Z-
dc.date.available2012-07-12T01:51:57Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Virology, 2008, v. 82 n. 20, p. 9928-9936en_US
dc.identifier.issn0022-538Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/152577-
dc.description.abstractAPOBEC3G (A3G) is a cytidine deaminase that restricts human immunodeficiency virus type 1 (HIV-1) replication. HIV-1 synthesizes a viral infectivity factor (Vif) to counter A3G restriction. Currently, it is poorly understood how A3G expression/activity is regulated by cellular factors. Here, we show that the prolyl isomerase Pin1 protein modulates A3G expression. Pin1 was found to be an A3G-interacting protein that reduces A3G expression and its incorporation into HIV-1 virion, thereby limiting A3G-mediated restriction of HIV-1. Intriguingly, HIV-1 infection modulates the phosphorylation state of Pin1, enhancing its ability to moderate A3G activity. These new findings suggest a potential Vif-independent way for HIV-1 to moderate the cellular action of A3G.en_US
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://jvi.asm.org/en_US
dc.relation.ispartofJournal of Virologyen_US
dc.titleHuman immunodeficiency virus type 1 replication and regulation of APOBEC3G by peptidyl prolyl isomerase Pin1en_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1128/JVI.01017-08en_US
dc.identifier.pmid18684817-
dc.identifier.scopuseid_2-s2.0-53749105363en_US
dc.identifier.volume82en_US
dc.identifier.issue20en_US
dc.identifier.spage9928en_US
dc.identifier.epage9936en_US
dc.identifier.isiWOS:000260109100012-
dc.publisher.placeUnited Statesen_US

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