Seo, Hyemin Lee, Icksoo Chung, Hak Suk Bae, Gyu-Un Chang, Minsun Song, Eunsook Kim, Min Jung 2024-01-20T04:03:13Z 2024-01-20T04:03:13Z 2021-09-04 2016-06 1976-8354 https://pubs.kist.re.kr/handle/201004/124019 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. English TAYLOR & FRANCIS LTD ATP5B regulates mitochondrial fission and fusion in mammalian cells Article 10.1080/19768354.2016.1188855 1 ANIMAL CELLS AND SYSTEMS, v.20, no.3, pp.157 - 164 ANIMAL CELLS AND SYSTEMS 20 3 157 164 N scie scopus kci ART002115982 000379549100006 2-s2.0-84976351051 Cell Biology Zoology Cell Biology Zoology Article HEART-MITOCHONDRIA SYNTHASE MORPHOLOGY NARP PATHOLOGY MUTATION SUBUNIT DISEASE Mitochondria ATP5B fission fusion