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@ARTICLE{Lechner:276875,
      author       = {S. Lechner and R. R. Steimbach$^*$ and L. Wang and M. L.
                      Deline and Y.-C. Chang and T. Fromme and M. Klingenspor and
                      P. Matthias and A. K. Miller$^*$ and G. Médard and B.
                      Kuster$^*$},
      title        = {{C}hemoproteomic target deconvolution reveals {H}istone
                      {D}eacetylases as targets of ({R})-lipoic acid.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-01184},
      pages        = {3548},
      year         = {2023},
      abstract     = {Lipoic acid is an essential enzyme cofactor in central
                      metabolic pathways. Due to its claimed antioxidant
                      properties, racemic (R/S)-lipoic acid is used as a food
                      supplement but is also investigated as a pharmaceutical in
                      over 180 clinical trials covering a broad range of diseases.
                      Moreover, (R/S)-lipoic acid is an approved drug for the
                      treatment of diabetic neuropathy. However, its mechanism of
                      action remains elusive. Here, we performed
                      chemoproteomics-aided target deconvolution of lipoic acid
                      and its active close analog lipoamide. We find that histone
                      deacetylases HDAC1, HDAC2, HDAC3, HDAC6, HDAC8, and HDAC10
                      are molecular targets of the reduced form of lipoic acid and
                      lipoamide. Importantly, only the naturally occurring
                      (R)-enantiomer inhibits HDACs at physiologically relevant
                      concentrations and leads to hyperacetylation of HDAC
                      substrates. The inhibition of HDACs by (R)-lipoic acid and
                      lipoamide explain why both compounds prevent stress granule
                      formation in cells and may also provide a molecular
                      rationale for many other phenotypic effects elicited by
                      lipoic acid.},
      cin          = {A390 / HD01 / MU01},
      ddc          = {500},
      cid          = {I:(DE-He78)A390-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)MU01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37322067},
      doi          = {10.1038/s41467-023-39151-8},
      url          = {https://inrepo02.dkfz.de/record/276875},
}