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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mitochondrial potassium channel Kv1.3 mediates Bax-induced apoptosis in lymphocytes
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Mitochondrial potassium channel Kv1.3 mediates Bax-induced apoptosis in lymphocytes

机译：线粒体钾通道Kv1.3介导Bax诱导的淋巴细胞凋亡

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摘要

The potassium channel Kv1.3 has recently been located to the inner mitochondrial membrane of lymphocytes. Here, we show that mouse and human cells that are genetically deficient in either Kv1.3 or transfected with siRNA to suppress Kv1.3-expression resisted apoptosis induced by several stimuli, including Bax over-expression. Retransfection of either Kv1.3 or a mitochondrial-targeted Kv1.3 restored cell death. Bax interacted with and functionally inhibited mitochondrial Kv1.3. Incubation of isolated Kv1.3-positive mitochondria with recombinant Bax, t-Bid, or toxins that bind to and inhibit Kv1.3 successively triggered hyperpolarization, formation of reactive oxygen species, release of cytochrome c, and marked depolarization. Kv1.3-deficient mitochondria were resistant to Bax, t-Bid, and the toxins. Mutation of Bax at K128, which corresponds to a conserved lysine in Kv1.3-inhibiting toxins, abrogated its effects on both Kv1.3 and mitochondria. These findings suggest that Bax mediates cytochrome c release and mitochondrial depolarization in lymphocytes, at least in part, via its interaction with mitochondrial Kv1.3.
机译：钾通道Kv1.3最近位于淋巴细胞的内部线粒体膜上。在这里，我们显示了在Kv1.3上遗传不足或用siRNA抑制Kv1.3表达转染的小鼠和人类细胞抵抗了由多种刺激（包括Bax过表达）诱导的凋亡。 Kv1.3或线粒体靶向的Kv1.3的重新转染可恢复细胞死亡。 Bax与线粒体Kv1.3相互作用并在功能上受到抑制。将分离的Kv1.3阳性线粒体与结合并抑制Kv1.3的重组Bax，t-Bid或毒素一起孵育会依次触发超极化，活性氧的形成，细胞色素c的释放和明显的去极化。 Kv1.3缺乏的线粒体对Bax，t-Bid和毒素具有抗性。 Bax在K128处的突变（对应于Kv1.3抑制毒素中保守的赖氨酸）消除了其对Kv1.3和线粒体的影响。这些发现表明，Bax至少部分地通过其与线粒体Kv1.3的相互作用介导淋巴细胞中细胞色素c的释放和线粒体去极化。

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