Loss of TAZ Boosts PPARγ to Cope with Insulin Resistance.
Where this comes from
- Record sourced from PubMed, PMID 31951568.
- Also identified by DOI 10.1016/j.cmet.2019.12.006.
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Abstract
In this issue of Cell Metabolism, El Ouarrat et al. identify the Hippo signaling terminal effector TAZ as an endogenous negative regulator of PPARγ, a master transcriptional regulator of lipid metabolism and insulin sensitivity. Selective destruction of TAZ in adipocytes lowers inflammation and restores insulin sensitivity and glucose homeostasis.
Medical subject headings
- Insulin Resistance