Other
19 Authors
- Deng S,
- Holland J,
- Jegga AG,
- Liu T,
- Wang B,
- Peng J,
- Perez-Tilve D,
- Gu H,
- Wang X,
- Nakamura T,
- Mu X,
- Essandoh K,
- Peng T,
- Yates E,
- McNamara RK,
- Li Y,
- Huang K,
- Fan GC,
- Chen J
| First Author | Peng J | Year | 2018 |
| Journal | Cell Rep | Volume | 23 |
| Issue | 12 | Pages | 3607-3620 |
| PubMed ID | 29925002 | Mgi Jnum | J:271250 |
| Mgi Id | MGI:6278478 | Doi | 10.1016/j.celrep.2018.05.065 |
| Citation | Peng J, et al. (2018) An Hsp20-FBXO4 Axis Regulates Adipocyte Function through Modulating PPARgamma Ubiquitination. Cell Rep 23(12):3607-3620 |
| abstractText | Exposure to cold temperature is well known to upregulate heat shock protein (Hsp) expression and recruit and/or activate brown adipose tissue and beige adipocytes in humans and animals. However, whether and how Hsps regulate adipocyte function for energy homeostatic responses is poorly understood. Here, we demonstrate a critical role of Hsp20 as a negative regulator of adipocyte function. Deletion of Hsp20 enhances non-shivering thermogenesis and suppresses inflammatory responses, leading to improvement of glucose and lipid metabolism under both chow diet and high-fat diet conditions. Mechanistically, Hsp20 controls adipocyte function by interacting with the subunit of the ubiquitin ligase complex, F-box only protein 4 (FBXO4), and regulating the ubiquitin-dependent degradation of peroxisome proliferation activated receptor gamma (PPARgamma). Indeed, Hsp20 deficiency mimics and enhances the pharmacological effects of the PPARgamma agonist rosiglitazone. Together, our findings suggest a role of Hsp20 in mediating adipocyte function by linking beta-adrenergic signaling to PPARgamma activity. |
