| First Author | Lauritzen I | Year | 2005 |
| Journal | EMBO Rep | Volume | 6 |
| Issue | 7 | Pages | 642-8 |
| PubMed ID | 15976821 | Mgi Jnum | J:99575 |
| Mgi Id | MGI:3583036 | Doi | 10.1038/sj.embor.7400449 |
| Citation | Lauritzen I, et al. (2005) Cross-talk between the mechano-gated K2P channel TREK-1 and the actin cytoskeleton. EMBO Rep 6(7):642-8 |
| abstractText | 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. |
