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Cross-talk between the mechano-gated K2P channel TREK-1 and the actin cytoskeleton.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Lauritzen, Inger Chemin, Jean Honoré, Eric Jodar, Martine Guy, Nicolas Lazdunski, Michel Patel, Amanda Jane |
| Copyright Year | 2005 |
| 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. |
| File Format | PDF HTM / HTML |
| DOI | 10.1038/sj.embor.7400449 |
| PubMed reference number | 15976821 |
| Journal | Medline |
| Volume Number | 6 |
| Issue Number | 7 |
| Alternate Webpage(s) | http://embor.embopress.org/content/embor/6/7/642.full.pdf |
| Alternate Webpage(s) | https://doi.org/10.1038/sj.embor.7400449 |
| Journal | EMBO reports |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
