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Sumihiro Kawajiri
Researcher at Juntendo University
Publications - 25
Citations - 3374
Sumihiro Kawajiri is an academic researcher from Juntendo University. The author has contributed to research in topics: Mitophagy & Mitochondrion. The author has an hindex of 13, co-authored 25 publications receiving 2858 citations. Previous affiliations of Sumihiro Kawajiri include University of California, Los Angeles.
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Journal ArticleDOI
PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy
Noriyuki Matsuda,Shigeto Sato,Kahori Shiba,Kei Okatsu,Keiko Saisho,Clement A. Gautier,Yu-shin Sou,Shinji Saiki,Sumihiro Kawajiri,Fumiaki Sato,Mayumi Kimura,Masaaki Komatsu,Nobutaka Hattori,Keiji Tanaka +13 more
TL;DR: Defective mitochondrial quality control is shown to be a mechanism for neurodegeneration in some forms of Parkinson's disease.
Journal ArticleDOI
Mechanisms of Mitochondrial Fission and Fusion
TL;DR: Three members of the Dynamin family are key components of the fission and fusion machineries and their functions are controlled by different sets of adaptor proteins on the surface of mitochondria and by a range of regulatory processes.
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Caffeine induces apoptosis by enhancement of autophagy via PI3K/Akt/mTOR/p70S6K inhibition
Shinji Saiki,Yukiko Sasazawa,Yoko Imamichi,Sumihiro Kawajiri,Takahiro Fujimaki,Isei Tanida,Hiroki Kobayashi,Fumiaki Sato,Shigeto Sato,Kei-Ichi Ishikawa,Masaya Imoto,Nobutaka Hattori +11 more
TL;DR: It is shown that caffeine increases both the levels of microtubule-associated protein 1 light chain 3-II and the number of autophagosomes and indicates a potential new target in the regulation of apoptosis.
Journal ArticleDOI
PINK1 is recruited to mitochondria with parkin and associates with LC3 in mitophagy
Sumihiro Kawajiri,Shinji Saiki,Shigeto Sato,Fumiaki Sato,Taku Hatano,Hiroto Eguchi,Nobutaka Hattori +6 more
TL;DR: This data indicates that direct interaction between LC3 and PINK1 and the anti bait coimmunoprecipitation mechanism is driven by a simple ‘spatially reprograming’ process.
Journal ArticleDOI
Mutations in Fis1 disrupt orderly disposal of defective mitochondria.
Qinfang Shen,Koji Yamano,Brian Head,Sumihiro Kawajiri,Sumihiro Kawajiri,Jesmine T. M. Cheung,Chunxin Wang,Jeong-Hoon Cho,Nobutaka Hattori,Richard J. Youle,Alexander M. van der Bliek +10 more
TL;DR: The mitochondrial fission protein Drp1 binds to Mff on mitochondria, followed by entry into a complex with Fis1 at the ER–mitochondrial interface, which acts in sequence with Mff to couple mitochondria fission with downstream degradation processes.