한빛사 논문
Abstract
Yongsung Kima, 1, Jeehye Parka, 1, Sunhong Kima, 1, Saera Songa, Seok-Kyu Kwonb, Sang-Hee Leec, Tohru Kitadad, Jin-Man Kime and Jongkyeong Chunga
aNational Creative Research Initiatives Center for Cell Growth Regulation and Department of Biological Sciences, Korea Advanced Institute of Science and Technology, 373-1 Kusong-Dong, Yusong-Gu, Taejon 305-701, Republic of Korea
bNational Creative Research Initiatives Center for Synaptogenesis and Department of Biological Sciences, Korea Advanced Institute of Science and Technology, 373-1 Kusong-dong, Yusong-Gu, Taejon 305-701, Republic of Korea
cDivision of Electron Microscopic Research, Korea Basic Science Institute, 52 Eoeun-Dong, Yusong-Gu, Taejon 305-333, Republic of Korea
dCenter for Neurologic Diseases, Brigham and Women’s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
evDepartment of Pathology, Chungnam National University School of Medicine, 640 Daesa-Dong, Chung-Gu, Taejon 301-721, Republic of Korea
Corresponding author. Fax: +82 42 350 8260.
1 These authors contributed equally to this work.
Abstract
PTEN-induced putative kinase 1 (PINK1) and Parkin, encoded by their respective genes associated with Parkinson’s disease (PD), are linked in a common pathway involved in the protection of mitochondrial integrity and function. However, the mechanism of their interaction at the biochemical level has not been investigated yet. Using both mammalian and Drosophila systems, we here demonstrate that the PINK1 kinase activity is required for its function in mitochondria. PINK1 regulates the localization of Parkin to the mitochondria in its kinase activity-dependent manner. In detail, Parkin phosphorylation by PINK1 on its linker region promotes its mitochondrial translocation, and the RING1 domain of Parkin is critical for this occurrence. These results demonstrate the biochemical relationship between PINK1, Parkin, and the mitochondria and thereby suggest the possible mechanism of PINK?Parkin-associated PD pathogenesis.
Keywords: Parkinson’s disease; PINK1; Parkin; Mitochondria; Phosphorylation
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