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SYK kinase mediates brown fat differentiation and activation.

Authors: Knoll, Marko  Winther, Sally  Natarajan, Anirudh  Yang, Huan  Jiang, Mengxi  Thiru, Prathapan  Shahsafaei, Aliakbar  Chavarria, Tony E  Lamming, Dudley W  Sun, Lei  Hansen, Jacob B  Lodish, Harvey F 
Citation: Knoll M, etal., Nat Commun. 2017 Dec 13;8(1):2115. doi: 10.1038/s41467-017-02162-3.
Pubmed: (View Article at PubMed) PMID:29235464
DOI: Full-text: DOI:10.1038/s41467-017-02162-3

Brown adipose tissue (BAT) metabolism influences glucose homeostasis and metabolic health in mice and humans. Sympathetic stimulation of ß-adrenergic receptors in response to cold induces proliferation, differentiation, and UCP1 expression in pre-adipocytes and mature brown adipocytes. Here we show that spleen tyrosine kinase (SYK) is upregulated during brown adipocyte differentiation and activated by ß-adrenergic stimulation. Deletion or inhibition of SYK, a kinase known for its essential roles in the immune system, blocks brown and white pre-adipocyte proliferation and differentiation in vitro, and results in diminished expression of Ucp1 and other genes regulating brown adipocyte function in response to ß-adrenergic stimulation. Adipocyte-specific SYK deletion in mice reduces BAT mass and BAT that developed consisted of SYK-expressing brown adipocytes that had escaped homozygous Syk deletion. SYK inhibition in vivo represses ß-agonist-induced thermogenesis and oxygen consumption. These results establish SYK as an essential mediator of brown fat formation and function.


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RGD Object Information
RGD ID: 13673776
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.