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@ARTICLE{BayindirBuchhalter:136847,
      author       = {I. Bayindir-Buchhalter and G. Wolff$^*$ and S. Lerch$^*$
                      and T. Sijmonsma$^*$ and M. Schuster$^*$ and J. Gronych$^*$
                      and A. T. Billeter and R. Babaei$^*$ and D. Krunic$^*$ and
                      L. Ketscher and N. Spielmann and M. Hrabe de Angelis and J.
                      L. Ruas and B. P. Müller-Stich and M. Heikenwalder$^*$ and
                      P. Lichter$^*$ and S. Herzig and A. Vegiopoulos$^*$},
      title        = {{C}ited4 is a sex-biased mediator of the antidiabetic
                      glitazone response in adipocyte progenitors.},
      journal      = {EMBO molecular medicine},
      volume       = {10},
      number       = {8},
      issn         = {1757-4684},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2018-01285},
      pages        = {e8613},
      year         = {2018},
      abstract     = {Most antidiabetic drugs treat disease symptoms rather than
                      adipose tissue dysfunction as a key pathogenic cause in the
                      metabolic syndrome and type 2 diabetes. Pharmacological
                      targeting of adipose tissue through the nuclear receptor
                      PPARg, as exemplified by glitazone treatments, mediates
                      efficacious insulin sensitization. However, a better
                      understanding of the context-specific PPARg responses is
                      required for the development of novel approaches with
                      reduced side effects. Here, we identified the
                      transcriptional cofactor Cited4 as a target and mediator of
                      rosiglitazone in human and murine adipocyte progenitor
                      cells, where it promoted specific sets of the
                      rosiglitazone-dependent transcriptional program. In mice,
                      Cited4 was required for the proper induction of thermogenic
                      expression by Rosi specifically in subcutaneous fat. This
                      phenotype had high penetrance in females only and was not
                      evident in beta-adrenergically stimulated browning.
                      Intriguingly, this specific defect was associated with
                      reduced capacity for systemic thermogenesis and compromised
                      insulin sensitization upon therapeutic rosiglitazone
                      treatment in female but not male mice. Our findings on
                      Cited4 function reveal novel unexpected aspects of the
                      pharmacological targeting of PPARg.},
      cin          = {A171 / F180 / B060 / L101 / W210},
      ddc          = {610},
      cid          = {I:(DE-He78)A171-20160331 / I:(DE-He78)F180-20160331 /
                      I:(DE-He78)B060-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)W210-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29973382},
      pmc          = {pmc:PMC6079535},
      doi          = {10.15252/emmm.201708613},
      url          = {https://inrepo02.dkfz.de/record/136847},
}