Ataxin-3 protects cells against H2O2-induced oxidative stress by enhancing the interaction between Bcl-XL and Bax
Ataxin-3 protects cells against H2O2-induced oxidative stress by enhancing the interaction between Bcl-XL and Bax
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DOI：
10.1016/j.neuroscience.2013.03.047
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发表时间：
2013-07
期刊：
影响因子：
3.3
通讯作者：
L. Zhou;H. Wang;P. Wang;H. Ren;D. Chen;Z. Ying;G. Wang
中科院分区：
文献类型：
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作者：
L. Zhou;H. Wang;P. Wang;H. Ren;D. Chen;Z. Ying;G. Wang
脊髓小脑性共济失调3型（SCA 3）是一种与多聚谷氨酰胺（polyQ）蛋白共济失调蛋白3相关的神经退行性疾病。共济失调蛋白-3是一种多功能蛋白质，但共济失调蛋白-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起着保护作用，对细胞氧化应激诱导的H2 O2在Bcl-XL依赖的方式。共济失调蛋白-3直接与Bcl-XL相互作用。ataxin-3的N-末端和Bcl-XL的C-末端是相互作用所必需的。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，共济失调蛋白-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。
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 H2O2in a Bcl-XL-dependent manner. Ataxin-3 directly interacts with Bcl-XL. The N-terminus of ataxin-3 and the C-terminus of Bcl-XLare essential for the interaction. Ataxin-3 promotes the interaction between Bcl-XLand 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-XLand Bax.