| First Author | Kwon KY | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 416 |
| Issue | 3-4 | Pages | 343-8 |
| PubMed ID | 22119190 | Mgi Jnum | J:179201 |
| Mgi Id | MGI:5301455 | Doi | 10.1016/j.bbrc.2011.11.038 |
| Citation | Kwon KY, et al. (2011) CCCP induces autophagy in an AMPK-independent manner. Biochem Biophys Res Commun 416(3-4):343-8 |
| abstractText | AMP-activated protein kinase (AMPK) is an important sensor of cellular energy status, and is involved in cell growth and autophagy through mammalian target of rapamycin complex 1 (mTORC1). Carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler, leads to AMPK activation and Parkin-dependent mitophagy, respectively. However, the detailed biochemical mechanism of how CCCP induces autophagy or mitophagy has not been investigated yet. Here, we showed that CCCP inhibits mTORC1 independently of AMPK, although CCCP induces AMPK activation. Using wild type (WT) and AMPKalpha1/alpha2 double knockout (DKO) MEFs, we observed that CCCP promotes endogenous LC3 lipidation and formation of RFP-LC3 puncta, indicating autophagosome or autolysosome, in an AMPK-independent manner. Finally, we also revealed that the percentage of CCCP-dependent colocalization between mitochondria and RFP-LC3 puncta is similar both in WT and AMPKalpha1/alpha2 DKO MEFs. Based on these data, we concluded that AMPK is not essential in regulation of CCCP-induced autopahgy including mitophagy. |
