Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 29, Issue 10, Pages 723-735Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2018.08.004
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Funding
- American Society of Bone and Mineral Research
- Harrington Discovery Institute
- National Institutes of Health (NIH) [K08 AR067285, R03 AR072150, R03 AR072903, 2R01 AR043369-22, 1R01CA222871-01, 1R01AR072304-01, 5P01 CA163222-05, P30 DK043351, U19 AI109725, R01 AI110498, P01 DK011794, P30 AR066261]
- Institut National de la Sante et de la Recherche Medicale, Centre National de la Recherche Scientifique, Universite Paris Descartes
- Societe francophone du diabete (SFD)
- Fondation pour la Recherche Medicale (FRM)
- Dr Miriam and Sheldon G. Adelson Medical Research Foundation
- Melanoma Research Alliance
- Helmsley Charitable Trust
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Salt-inducible kinases (SIKs) represent a subfamily of AMP-activated protein kinase (AMPK) family kinases. Initially named because SIK1 (the founding member of this kinase family) expression is regulated by dietary salt intake in the adrenal gland, it is now apparent that a major biological role of these kinases is to control gene expression in response to extracellular cues that increase intracellular levels of cAMP. Here, we review four physiologically relevant examples of how cAMP signaling impinges upon SIK cellular function. By focusing on examples of cAMP-mediated SIK regulation in gut myeloid cells, bone, liver, and skin, we highlight recent advances in G protein-coupled receptor (GPCR) signal transduction. New knowledge regarding the role of SIKs in GPCR signaling has led to therapeutic applications of novel small molecule SIK inhibitors.
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