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http://purl.uniprot.org/citations/24121441http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24121441http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24121441http://www.w3.org/2000/01/rdf-schema#comment"HIV-1 replication can be inhibited by type I interferon (IFN), and the expression of a number of gene products with anti-HIV-1 activity is induced by type I IFN. However, none of the known antiretroviral proteins can account for the ability of type I IFN to inhibit early, preintegration phases of the HIV-1 replication cycle in human cells. Here, by comparing gene expression profiles in cell lines that differ in their ability to support the inhibitory action of IFN-α at early steps of the HIV-1 replication cycle, we identify myxovirus resistance 2 (MX2) as an interferon-induced inhibitor of HIV-1 infection. Expression of MX2 reduces permissiveness to a variety of lentiviruses, whereas depletion of MX2 using RNA interference reduces the anti-HIV-1 potency of IFN-α. HIV-1 reverse transcription proceeds normally in MX2-expressing cells, but 2-long terminal repeat circular forms of HIV-1 DNA are less abundant, suggesting that MX2 inhibits HIV-1 nuclear import, or destabilizes nuclear HIV-1 DNA. Consistent with this notion, mutations in the HIV-1 capsid protein that are known, or suspected, to alter the nuclear import pathways used by HIV-1 confer resistance to MX2, whereas preventing cell division increases MX2 potency. Overall, these findings indicate that MX2 is an effector of the anti-HIV-1 activity of type-I IFN, and suggest that MX2 inhibits HIV-1 infection by inhibiting capsid-dependent nuclear import of subviral complexes."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.org/dc/terms/identifier"doi:10.1038/nature12653"xsd:string
http://purl.uniprot.org/citations/24121441http://purl.org/dc/terms/identifier"doi:10.1038/nature12653"xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Yamashita M."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Yamashita M."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Rice C.M."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Rice C.M."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Wilson S.J."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Wilson S.J."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Bieniasz P.D."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Bieniasz P.D."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Kane M."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Kane M."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Schoggins J.W."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Schoggins J.W."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Hatziioannou T."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Hatziioannou T."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Kutluay S.B."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Kutluay S.B."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Zang T."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Zang T."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Bitzegeio J."xsd:string
http://purl.uniprot.org/citations/24121441http://purl.uniprot.org/core/author"Bitzegeio J."xsd:string