Apoptotic proteins Reaper and Grim induce stable inactivation in voltage-gated K+ channels.
Apoptotic proteins Reaper and Grim induce stable inactivation in voltage-gated K+ channels.
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DOI：
10.1073/pnas.95.20.11703
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发表时间：
1998-09
影响因子：
11.1
通讯作者：
V. Avdonin;J. Kasuya;M. Ciorba;B. Kaplan;Toshinori Hoshi;Linda E. Iverson
中科院分区：
文献类型：
--
作者：
V. Avdonin;J. Kasuya;M. Ciorba;B. Kaplan;Toshinori Hoshi;Linda E. Iverson
Drosophila genes reaper, grim, and head-involution-defective (hid) induce apoptosis in several cellular contexts. N-terminal sequences of these proteins are highly conserved and are similar to N-terminal inactivation domains of voltage-gated potassium (K+) channels. Synthetic Reaper and Grim N terminus peptides induced fast inactivation of Shaker-type K+ channels when applied to the cytoplasmic side of the channel that was qualitatively similar to the inactivation produced by other K+ channel inactivation particles. Mutations that reduce the apoptotic activity of Reaper also reduced the synthetic peptide's ability to induce channel inactivation, indicating that K+ channel inactivation correlated with apoptotic activity. Coexpression of Reaper RNA or direct injection of full length Reaper protein caused near irreversible block of the K+ channels. These results suggest that Reaper and Grim may participate in initiating apoptosis by stably blocking K+ channels.
