Supplementary Materials

Supplementary Materials for:

Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

Rohollah Babaei, Maximilian Schuster, Irina Meln, Sarah Lerch, Rayane A. Ghandour, Didier F. Pisani, Irem Bayindir-Buchhalter, Julia Marx, Shuang Wu, Gabriele Schoiswohl, Adrian T. Billeter, Damir Krunic, Jan Mauer, Yun-Hee Lee, James G. Granneman, Lars Fischer, Beat P. Müller-Stich, Ez-Zoubir Amri, Erin E. Kershaw, Mathias Heikenwälder, Stephan Herzig,* Alexandros Vegiopoulos*

*Corresponding author. Email: a.vegiopoulos{at}dkfz.de (A.V.); stephan.herzig{at}helmholtz-muenchen.de (S.H.)

This PDF file includes:

  • Fig. S1. Continuous inhibition of Jak1/2 activity disrupts white and beige adipocyte differentiation of defined murine progenitors.
  • Fig. S2. Jak activity is required for human beige adipocyte differentiation.
  • Fig. S3. The Jak family of kinases promote progenitor activation and adipogenic commitment before the induction of Pparg and its targets.
  • Fig. S4. The Jak family of kinases inhibit autocrine and paracrine TGFβ signaling to permit commitment and thermogenic differentiation of adipocyte progenitors.
  • Fig. S5. Stat3 inhibits TGFβ signaling in progenitors and is required for progenitor differentiation.
  • Fig. S6. Lipolysis-dependent Jak/Stat3 activation and Tgfb3 regulation at the onset of β-adrenergic–induced adipose tissue remodeling.
  • Fig. S7. IL-11 triggers the Jak/Stat3-Tgfb3 axis in progenitors and in adipose tissue.
  • Table S1. Sequence of primers used for qPCR analysis.

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