ATP5B regulates mitochondrial fission and fusion in mammalian cellsopen access
- Authors
- Seo, Hyemin; Lee, Icksoo; Chung, Hak Suk; Bae, Gyu-Un; Chang, Minsun; Song, Eunsook; Kim, Min Jung
- Issue Date
- Jun-2016
- Publisher
- TAYLOR & FRANCIS LTD
- Keywords
- Mitochondria; ATP5B; fission; fusion
- Citation
- ANIMAL CELLS AND SYSTEMS, v.20, no.3, pp 157 - 164
- Pages
- 8
- Journal Title
- ANIMAL CELLS AND SYSTEMS
- Volume
- 20
- Number
- 3
- Start Page
- 157
- End Page
- 164
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9786
- DOI
- 10.1080/19768354.2016.1188855
- ISSN
- 1976-8354
2151-2485
- Abstract
- Mitochondria are essential organelles that produce ATP and regulate cell growth, proliferation, and cell death. To maintain homeostasis, fusion and fission of mitochondria must be strictly regulated. Even though oligomerization of ATP synthase could affect the mitochondrial morphology, the exact mechanism is not clear. We confirmed that structure and function of ATP5B, which is a major component of the catalytic center of ATP synthase complexes, are closely connected to the mitochondrial morphology. ATP5B itself can enhance elongation of mitochondria. Moreover, mutations of the threonine residue at -barrel domain, and the serine residue at nucleotide-binding domain of ATP5B, produce the opposite effect on the fission and fusion of mitochondrial networks. Here, we demonstrate that ATP5B is clearly involved in the mechanism of regulation for mitochondrial fusion and fission in mammalian cells.
- Files in This Item
-
Go to Link
- Appears in
Collections - 이과대학 > 생명시스템학부 > 1. Journal Articles
- 약학대학 > 약학부 > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.