STK38 is a PPARγ-interacting protein promoting adipogenesis

Adipocyte. 2021 Dec;10(1):524-531. doi: 10.1080/21623945.2021.1980257.

Abstract

Peroxisome proliferator-activated receptor-γ (PPARγ) is the master regulator of adipogenesis, but knowledge about how PPARγ is regulated at the protein level is very limited. We aimed to identify PPARγ-interacting proteins which modulate PPARγ's protein levels and transactivating activities in human adipocytes. We expressed Flag-tagged PPARγ in human preadipocytes as bait to capture PPARγ-associated proteins, followed by mass spectroscopy and proteomics analysis, which identified serine/threonine kinase 38 (STK38) as a major PPARγ-associated protein. Protein pulldown studies confirmed this protein-protein interaction in transfected cells, and reporter assays demonstrated that STK38 enhanced PPARγ's transactivating activities without requiring STK38's kinase activity. In cell-based assays, STK38 increased PPARγ protein stability, extending PPARγ's half-life from ~1.08 to 1.95 h. Notably, in human preadipocytes, the overexpression of STK38 enhanced adipogenesis, whereas knockdown impaired the process in a PPARγ-dependent manner. Thus, we discovered that STK38 is a novel PPARγ-cofactor promoting adipogenesis, likely through stabilization of PPARγ.

Keywords: PPARγ; STK38; cofactors and adipocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism
  • Adipogenesis*
  • Humans
  • PPAR gamma* / metabolism
  • Phosphorylation
  • Protein Serine-Threonine Kinases* / genetics

Substances

  • PPAR gamma
  • Protein Serine-Threonine Kinases
  • STK38 protein, human

Grants and funding

The work was partially supported by Maryland Stem Cell Research Fund.