Atg4BC74A hampers autophagosome closure: A useful protein for inhibiting autophagy

Naonobu Fujita, Takeshi Noda, Tamotsu Yoshimori

    研究成果: Article査読

    25 被引用数 (Scopus)

    抄録

    Recently we have reported that overexpression of an inactive mutant of Atg4B, a protease that processes proLC3 paralogues, inhibits lipidation of LC3 paralogues and autophagic degradation in mammalian cell. Through a mechanistic analysis, it was revealed that excess Atg4B mutant sequesters LC3 paralogues and blocks formation of Atg7-LC3 intermediate. Upon trap of LC3 paralogues, Atg5-positive autophagic structures accumulated. The structures are defective in the final closing step in autophagosome formation. The ability of the excess Atg4B mutant to inhibit autophagy provides not only an opportunity for further analysis of the LC3 system but also a useful tool available for a wide variety of experimental systems used in the study of autophagy.

    本文言語English
    ページ(範囲)88-89
    ページ数2
    ジャーナルAutophagy
    5
    1
    出版ステータスPublished - 2009 1 1

    ASJC Scopus subject areas

    • 分子生物学
    • 細胞生物学

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