% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Boehm:274207,
      author       = {D. Boehm and V. Lam and M. Schnölzer$^*$ and M. Ott},
      title        = {{T}he lysine methyltransferase {SMYD}5 amplifies {HIV}-1
                      transcription and is post-transcriptionally upregulated by
                      {T}at and {USP}11.},
      journal      = {Cell reports},
      volume       = {42},
      number       = {3},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-00493},
      pages        = {112234},
      year         = {2023},
      abstract     = {A 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.},
      keywords     = {CP: Microbiology (Other) / HIV-1 (Other) / SMYD5 (Other) /
                      TAR RNA (Other) / Tat (Other) / USP11 (Other) / latency
                      (Other)},
      cin          = {B100},
      ddc          = {610},
      cid          = {I:(DE-He78)B100-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36897778},
      doi          = {10.1016/j.celrep.2023.112234},
      url          = {https://inrepo02.dkfz.de/record/274207},
}