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http://purl.uniprot.org/citations/22791714http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22791714http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22791714http://www.w3.org/2000/01/rdf-schema#comment"The apolipoprotein-B-mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G or A3G) is a potent restrictive factor for human immunodeficiency virus type 1 (HIV-1) and many other retroviruses. It belongs to the cytidine deaminase family. Recent studies have shown that A3G significantly inhibits microRNA (miRNA)-mediated repression of translation. However, the mechanism underlying this action must be clarified. In this report, we have demonstrated that A3G counteracts miRNA-mediated repression of translation by inhibiting the interaction between moloney leukemia virus 10 (MOV10) protein and Argonaute-2 (AGO2), causing either abnormal assembly or abnormal maturation of miRNA-inducing silencing complex (miRISC). Through a series of MOV10 deletions, we found that A3G binds to a domain at the C terminus in MOV10, where it competitively inhibits the binding of AGO2 to that same domain. The interaction between A3G and MOV10 relies on its association with a small RNA named 7SL RNA. The A3G mutant W127L, which is unable to bind to 7SL RNA, shows significantly incapability to counteract the miRNA-mediated repression of translation. Our data demonstrate a novel mechanism involved in the regulation of miRISC activity. Although both A3G and MOV10 belong to the interferon antiviral system and inhibit HIV-1 and other retroviruses, their opposing effects on the cellular miRNA activity suggest that they play much more complicated regulatory roles in various cellular functions."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m112.354001"xsd:string
http://purl.uniprot.org/citations/22791714http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m112.354001"xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Liu B."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Liu B."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Liu C."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Liu C."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Luo H."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Luo H."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Zhang P."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Zhang P."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Yang B."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Yang B."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Huang F."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/author"Huang F."xsd:string
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22791714http://purl.uniprot.org/core/date"2012"xsd:gYear