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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
Watashi, KKhan, MYedavalli, VRKYeung, MLStrebe, KJeang, KT
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?
DOI: http://dx.doi.org/10.1128/JVI.01017-08
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
0022-538X
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.378
ISI Accession Number ID
WOS:000260109100012
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
dc.identifier.issnl0022-538X-

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