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• W2000679662 abstract "Although dispensable in vitro, HIV Nef enables high-level viral replication in infected hosts by an as yet unexplained mechanism. Previously, we proposed that Nef functionally cooperates with the viral transactivator Tat by derepressing the viral promoter via a Nef-associated kinase complex (NAKC). Here, we demonstrate that hnRNP-K, a host factor thought to facilitate crosstalk between kinases and gene expression, interacts with Nef and, as part of NAKC, nucleates Nef-interacting kinases, including Lck, PKCdelta, and PI-3 kinase, leading to Lck and Erk1/2 activation. This strongly increased HIV transcription, which depended on Tat and the NF-kB motif in the viral promoter, but not on NF-kB activation. Depletion of hnRNP-K in a Jurkat model of HIV latency increased Erk1/2 activity and greatly augmented HIV reactivating stimuli. We conclude that hnRNP-K coordinates membrane signaling with transcriptional derepression through Erk1/2 and is targeted by HIV to enable Tat-mediated transcription." @default.
• W2000679662 created "2016-06-24" @default.
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• W2000679662 date "2008-10-01" @default.
• W2000679662 modified "2023-09-23" @default.
• W2000679662 title "HIV Nef Enhances Tat-Mediated Viral Transcription through a hnRNP-K-Nucleated Signaling Complex" @default.
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• W2000679662 doi "https://doi.org/10.1016/j.chom.2008.08.013" @default.
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