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Research Article

The Loss of PGAM5 Suppresses the Mitochondrial Degeneration Caused by Inactivation of PINK1 in Drosophila

  • Yuzuru Imai equal contributor mail,

    equal contributor Contributed equally to this work with: Yuzuru Imai, Tomoko Kanao

    yimai@idac.tohoku.ac.jp

    Affiliation: Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan

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  • Tomoko Kanao equal contributor,

    equal contributor Contributed equally to this work with: Yuzuru Imai, Tomoko Kanao

    Affiliation: Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan

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  • Tomoyo Sawada,

    Affiliation: Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan

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  • Yoshito Kobayashi,

    Affiliation: Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan

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  • Yasuhiro Moriwaki,

    Affiliation: Department of Pharmacology, Faculty of Pharmacy, Keio University, Tokyo, Japan

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  • Yosuke Ishida,

    Affiliation: Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan

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  • Kohsuke Takeda,

    Affiliation: Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan

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  • Hidenori Ichijo,

    Affiliation: Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan

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  • Bingwei Lu,

    Affiliation: Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America

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  • Ryosuke Takahashi

    Affiliation: Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan

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  • Published: December 02, 2010
  • DOI: 10.1371/journal.pgen.1001229

About the Authors

Yuzuru Imai, Tomoko Kanao
Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan
Tomoyo Sawada, Yoshito Kobayashi, Ryosuke Takahashi
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
Yasuhiro Moriwaki
Department of Pharmacology, Faculty of Pharmacy, Keio University, Tokyo, Japan
Yosuke Ishida, Kohsuke Takeda, Hidenori Ichijo
Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan
Bingwei Lu
Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America

Corresponding Author

Email: yimai@idac.tohoku.ac.jp

Competing Interests

The authors have declared that no competing interests exist.

Author Contributions

Conceived and designed the experiments: Y Imai, T Kanao. Performed the experiments: Y Imai, T Kanao, T Sawada, Y Kobayashi, Y Moriwaki. Analyzed the data: Y Imai, T Kanao, T Sawada. Contributed reagents/materials/analysis tools: Y Moriwaki, Y Ishida, K Takeda, H Ichijo, B Lu, R Takahashi. Wrote the paper: Y Imai.