| First Author | Kim HJ | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 464 |
| Issue | 4 | Pages | 1235-40 |
| PubMed ID | 26210454 | Mgi Jnum | J:232518 |
| Mgi Id | MGI:5779473 | Doi | 10.1016/j.bbrc.2015.07.111 |
| Citation | Kim HJ, et al. (2015) HDAC6 maintains mitochondrial connectivity under hypoxic stress by suppressing MARCH5/MITOL dependent MFN2 degradation. Biochem Biophys Res Commun 464(4):1235-40 |
| abstractText | Mitochondria undergo fusion and fission in response to various metabolic stresses. Growing evidences have suggested that the morphological change of mitochondria by fusion and fission plays a critical role in protecting mitochondria from metabolic stresses. Here, we showed that hypoxia treatment could induce interaction between HDAC6 and MFN2, thus protecting mitochondrial connectivity. Mechanistically, we demonstrated that a mitochondrial ubiquitin ligase MARCH5/MITOL was responsible for hypoxia-induced MFN2 degradation in HDAC6 deficient cells. Notably, genetic abolition of HDAC6 in amyotrophic lateral sclerosis model mice showed MFN2 degradation with MARCH5 induction. Our results indicate that HDAC6 is a critical regulator of MFN2 degradation by MARCH5, thus protecting mitochondrial connectivity from hypoxic stress. |
