在高尔基体中捕获CDC42 c末端变异体驱动pyrin炎性体过度活化

The Tokushima journal of experimental medicine Pub Date : 2022-04-28 DOI:10.1084/jem.20211889

Masahiko Nishitani-Isa, Kojiro Mukai, Y. Honda, H. Nihira, Takayuki Tanaka, H. Shibata, K. Kodama, E. Hiejima, K. Izawa, Yuri Kawasaki, M. Osawa, Yu Katata, Sachiko Onodera, Tatsuya Watanabe, T. Uchida, S. Kure, J. Takita, O. Ohara, M. Saito, R. Nishikomori, T. Taguchi, Y. Sasahara, T. Yasumi

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引用次数: 10

摘要

利用携带CDC42R186C的诱导多能干细胞，在高尔基体中捕获CDC42 c端变体，通过一种独立于GTPase活性的机制，促进pyrin炎性体的组装，从而引发自身炎症。

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Trapping of CDC42 C-terminal variants in the Golgi drives pyrin inflammasome hyperactivation

Using induced pluripotent stem cells carrying CDC42R186C, trapping of CDC42 C-terminal variants within the Golgi apparatus is shown to trigger autoinflammation by promoting pyrin inflammasome assembly through a mechanism independent of their GTPase activity.

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The Tokushima journal of experimental medicine

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