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000274207 1001_ $$aBoehm, Daniela$$b0
000274207 245__ $$aThe lysine methyltransferase SMYD5 amplifies HIV-1 transcription and is post-transcriptionally upregulated by Tat and USP11.
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000274207 520__ $$aA successful HIV-1 cure strategy may require enhancing HIV-1 latency to silence HIV-1 transcription. Modulators of gene expression show promise as latency-promoting agents in vitro and in vivo. Here, we identify Su(var)3-9, enhancer-of-zeste, and trithorax (SET) and myeloid, Nervy, and DEAF-1 (MYND) domain-containing protein 5 (SMYD5) as a host factor required for HIV-1 transcription. SMYD5 is expressed in CD4+ T cells and activates the HIV-1 promoter with or without the viral Tat protein, while knockdown of SMYD5 decreases HIV-1 transcription in cell lines and primary T cells. SMYD5 associates in vivo with the HIV-1 promoter and binds the HIV trans-activation response (TAR) element RNA and Tat. Tat is methylated by SMYD5 in vitro, and in cells expressing Tat, SMYD5 protein levels are increased. The latter requires expression of the Tat cofactor and ubiquitin-specific peptidase 11 (USP11). We propose that SMYD5 is a host activator of HIV-1 transcription stabilized by Tat and USP11 and, together with USP11, a possible target for latency-promoting therapy.
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000274207 650_7 $$2Other$$aCP: Microbiology
000274207 650_7 $$2Other$$aHIV-1
000274207 650_7 $$2Other$$aSMYD5
000274207 650_7 $$2Other$$aTAR RNA
000274207 650_7 $$2Other$$aTat
000274207 650_7 $$2Other$$aUSP11
000274207 650_7 $$2Other$$alatency
000274207 7001_ $$aLam, Victor$$b1
000274207 7001_ $$0P:(DE-He78)38b33779833838a98c2a241ce465fb07$$aSchnölzer, Martina$$b2
000274207 7001_ $$aOtt, Melanie$$b3
000274207 773__ $$0PERI:(DE-600)2649101-1$$a10.1016/j.celrep.2023.112234$$gVol. 42, no. 3, p. 112234 -$$n3$$p112234$$tCell reports$$v42$$x2211-1247$$y2023
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