Ataxin-3 通过增强 Bcl-X(L) 和 Bax 之间的相互作用，保护细胞免受 H2O2 诱导的氧化应激。
Ataxin-3 protects cells against H2O2-induced oxidative stress by enhancing the interaction between Bcl-X(L) and Bax.
机构信息
Laboratory of Molecular Neuropathology, Key Laboratory of Brain Function and Disease, School of Life Sciences, University of Science & Technology of China, Chinese Academy of Sciences, Hefei, Anhui 230027, China.
出版信息
Neuroscience. 2013 Jul 23;243:14-21. doi: 10.1016/j.neuroscience.2013.03.047. Epub 2013 Apr 2.
Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disorder associated with polyglutamine (polyQ) protein ataxin-3. Ataxin-3 is a multi-functional protein, but the precise mechanisms underlying the cellular functions of ataxin-3 remain to be elucidated. Here we demonstrate that ataxin-3 plays a protective role against cellular oxidative stress induced by H2O2 in a Bcl-XL-dependent manner. Ataxin-3 directly interacts with Bcl-XL. The N-terminus of ataxin-3 and the C-terminus of Bcl-XL are essential for the interaction. Ataxin-3 promotes the interaction between Bcl-XL and Bax, but does not affect the ubiquitination and degradation of Bcl-XL. Our data suggest that ataxin-3 plays an important role in regulating the Bcl-XL-Bax-mediated anti-oxidative response by modulating the interaction between Bcl-XL and Bax.
脊髓小脑共济失调 3 型（SCA3）是一种与多聚谷氨酰胺（polyQ）蛋白 ataxin-3 相关的神经退行性疾病。ataxin-3 是一种多功能蛋白，但 ataxin-3 的细胞功能的确切机制仍有待阐明。在这里，我们证明 ataxin-3 以 Bcl-XL 依赖的方式发挥对 H2O2 诱导的细胞氧化应激的保护作用。ataxin-3 直接与 Bcl-XL 相互作用。ataxin-3 的 N 端和 Bcl-XL 的 C 端对于相互作用是必需的。ataxin-3 促进 Bcl-XL 和 Bax 之间的相互作用，但不影响 Bcl-XL 的泛素化和降解。我们的数据表明，ataxin-3 通过调节 Bcl-XL 和 Bax 之间的相互作用，在调节 Bcl-XL-Bax 介导的抗氧化反应中发挥重要作用。
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