Protein kinase C bound with A-kinase anchoring protein is involved in muscarinic receptor-activated modulation of M-type KCNQ potassium channels.
作者： Haruhiro Higashida , Naoto Hoshi , Jia-Sheng Zhang , Shigeru Yokoyama , Minako Hashii
DOI: 10.1016/J.NEURES.2004.11.009
关键词:
摘要: The second messenger for closure of M/KCNQ potassium channels in post-ganglionic neurons and central had remained as a 'mystery the neuroscience field' over 25 years. However, recently details pathway leading from muscarinic acetylcholine receptor (mAChR)-stimulation to suppression M/KCNQ-current were discovered. A key molecule is A-kinase anchoring protein (AKAP; AKAP79 human, or its rat homolog, AKAP150) which forms trimeric complex with kinase C (PKC) KCNQ channels. 150 serves an adapter that brings anchored C-kinase substrate channel permit rapid 'definitive' phosphorylation serine residues, resulting avoidance signal dispersion. Thus, these findings suggest mAChR-induced short-term modulation (or memory) does occur within already well-integrated molecular complex, without accompanying Hebbian synapse plasticity. before this identity confirmed, many other modulators affect M-currents remain be addressed intriguing issues.
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