| Literature DB >> 10707089 |
I Dzhura1, Y Wu, R J Colbran, J R Balser, M E Anderson.
Abstract
A dynamic positive feedback mechanism, known as 'facilitation', augments L-type calcium-ion currents (ICa) in response to increased intracellular Ca2+ concentrations. The Ca2+-binding protein calmodulin (CaM) has been implicated in facilitation, but the single-channel signature and the signalling events underlying Ca2+/CaM-dependent facilitation are unknown. Here we show that the Ca2+/CaM-dependent protein kinase II (CaMK) is necessary and possibly sufficient for ICa facilitation. CaMK induces a channel-gating mode that is characterized by frequent, long openings of L-type Ca2+ channels. We conclude that CaMK-mediated phosphorylation is an essential signalling event in triggering Ca2+/CaM-dependent ICa facilitation.Entities:
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Year: 2000 PMID: 10707089 DOI: 10.1038/35004052
Source DB: PubMed Journal: Nat Cell Biol ISSN: 1465-7392 Impact factor: 28.824