Fast inactivation of Shal (K(v)4) K+ channels is regulated by the novel interactor SKIP3 in Drosophila neurons.
Fast inactivation of Shal (K(v)4) K+ channels is regulated by the novel interactor SKIP3 in Drosophila neurons.
复制标题
SHAL的快速失活（K（v）4）K+通道受果蝇神经元中新型的Itsporter Skip3的调节。
DOI：
10.1016/j.mcn.2009.05.003
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发表时间：
2009-09
影响因子：
3.5
通讯作者：
Tsunoda, Susan
中科院分区：
文献类型：
--
作者：
Diao, Fengqiu;Waro, Girma;Tsunoda, Susan
Shal K+ (Kv4) channels across species carry the major A-type K+ current present in neurons. Shal currents are activated by small EPSPs and modulate post-synaptic potentials, backpropagation of action potentials, and induction of LTP. Fast inactivation of Shal channels regulates the impact of this post-synaptic modulation. Here, we introduce SKIP3, as the first protein interactor of Drosophila Shal K+ channels. The SKIP gene encodes three isoforms with multiple protein-protein interaction domains. SKIP3 is nervous system specific and co-localizes with Shal channels in neuronal cell bodies, and in puncta along processes. Using a genetic deficiency of SKIP, we show that the proportion of neurons displaying a very fast inactivation, consistent with Shal channels exclusively in a “fast” gating mode, is increased in the absence of SKIP3. As a scaffold-like protein, SKIP3 is likely to lead to the identification of a novel regulatory complex that modulates Shal channel inactivation.
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Bhattacharjya, S;Xu, P;Ni, F
通讯作者：
Ni, F
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Bowie, JU
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Imaizumi, Y
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