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• W1973272114 abstract "TREK-1 (KCNK2) is a K(2P) channel that is highly expressed in fetal neurons. This K(+) channel is opened by a variety of stimuli, including membrane stretch and cellular lipids. Here, we show that the expression of TREK-1 markedly alters the cytoskeletal network and induces the formation of actin- and ezrin-rich membrane protrusions. The genetic inactivation of TREK-1 significantly alters the growth cone morphology of cultured embryonic striatal neurons. Cytoskeleton remodelling is crucially dependent on the protein kinase A phosphorylation site S333 and the interactive proton sensor E306, but is independent of channel permeation. Conversely, the actin cytoskeleton tonically represses TREK-1 mechano-sensitivity. Thus, the dialogue between TREK-1 and the actin cytoskeleton might influence both synaptogenesis and neuronal electrogenesis." @default.
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• W1973272114 date "2005-07-01" @default.
• W1973272114 modified "2023-10-18" @default.
• W1973272114 title "Cross‐talk between the mechano‐gated K _2P channel TREK‐1 and the actin cytoskeleton" @default.
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• W1973272114 doi "https://doi.org/10.1038/sj.embor.7400449" @default.
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