| First Author | Shinoda K | Year | 2015 |
| Journal | Cell Metab | Volume | 22 |
| Issue | 6 | Pages | 997-1008 |
| PubMed ID | 26525534 | Mgi Jnum | J:235826 |
| Mgi Id | MGI:5803762 | Doi | 10.1016/j.cmet.2015.09.029 |
| Citation | Shinoda K, et al. (2015) Phosphoproteomics Identifies CK2 as a Negative Regulator of Beige Adipocyte Thermogenesis and Energy Expenditure. Cell Metab 22(6):997-1008 |
| abstractText | Catecholamines promote lipolysis both in brown and white adipocytes, whereas the same stimuli preferentially activate thermogenesis in brown adipocytes. Molecular mechanisms for the adipose-selective activation of thermogenesis remain poorly understood. Here, we employed quantitative phosphoproteomics to map global and temporal phosphorylation profiles in brown, beige, and white adipocytes under beta3-adrenenoceptor activation and identified kinases responsible for the adipose-selective phosphorylation profiles. We found that casein kinase2 (CK2) activity is preferentially higher in white adipocytes than brown/beige adipocytes. Genetic or pharmacological blockade of CK2 in white adipocytes activates the thermogenic program in response to cAMP stimuli. Such activation is largely through reduced CK2-mediated phosphorylation of class I HDACs. Notably, inhibition of CK2 promotes beige adipocyte biogenesis and leads to an increase in whole-body energy expenditure and ameliorates diet-induced obesity and insulin resistance. These results indicate that CK2 is a plausible target to rewire the beta3-adrenenoceptor signaling cascade that promotes thermogenesis in adipocytes. |
