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@ARTICLE{Babaei:132784,
      author       = {R. Babaei$^*$ and M. Schuster$^*$ and I. Meln$^*$ and S.
                      Lerch$^*$ and R. A. Ghandour and D. F. Pisani and I.
                      Bayindir-Buchhalter$^*$ and J. Marx$^*$ and S. Wu$^*$ and G.
                      Schoiswohl and A. T. Billeter and D. Krunic$^*$ and J. Mauer
                      and Y.-H. Lee and J. G. Granneman and L. Fischer and B. P.
                      Müller-Stich and E.-Z. Amri and E. E. Kershaw and M.
                      Heikenwälder$^*$ and S. Herzig and A. Vegiopoulos$^*$},
      title        = {{J}ak-{TGF}β cross-talk links transient adipose tissue
                      inflammation to beige adipogenesis.},
      journal      = {Science signaling},
      volume       = {11},
      number       = {527},
      issn         = {1937-9145},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2018-00428},
      pages        = {eaai7838 -},
      year         = {2018},
      abstract     = {The transient activation of inflammatory networks is
                      required for adipose tissue remodeling including the
                      'browning' of white fat in response to stimuli such as
                      β3-adrenergic receptor activation. In this process, white
                      adipose tissue acquires thermogenic characteristics through
                      the recruitment of so-called beige adipocytes. We
                      investigated the downstream signaling pathways impinging on
                      adipocyte progenitors that promote de novo formation of
                      adipocytes. We showed that the Jak family of kinases
                      controlled TGFβ signaling in the adipose tissue
                      microenvironment through Stat3 and thereby adipogenic
                      commitment, a function that was required for beige adipocyte
                      differentiation of murine and human progenitors. Jak/Stat3
                      inhibited TGFβ signaling to the transcription factors Srf
                      and Smad3 by repressing local Tgfb3 and Tgfb1 expression
                      before the core transcriptional adipogenic cascade was
                      activated. This pathway cross-talk was triggered in stromal
                      cells by ATGL-dependent adipocyte lipolysis and a transient
                      wave of IL-6 family cytokines at the onset of adipose tissue
                      remodeling induced by β3-adrenergic receptor stimulation.
                      Our results provide insight into the activation of adipocyte
                      progenitors and are relevant for the therapeutic targeting
                      of adipose tissue inflammatory pathways.},
      cin          = {A171 / F180 / W210},
      ddc          = {500},
      cid          = {I:(DE-He78)A171-20160331 / I:(DE-He78)F180-20160331 /
                      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:29692363},
      doi          = {10.1126/scisignal.aai7838},
      url          = {https://inrepo02.dkfz.de/record/132784},
}