論文

査読有り
2005年6月

K-ATP channel interaction with adenine nucleotides

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
  • M Matsuo
  • ,
  • Y Kimura
  • ,
  • K Ueda

38
6
開始ページ
907
終了ページ
916
記述言語
英語
掲載種別
DOI
10.1016/j.yjmcc.2004.11.021
出版者・発行元
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD

ATP-sensitive potassium (K-ATP) channels are regulated by adenine nucleotides to convert changes in cellular metabolic levels into membrane excitability. Hence. elucidation of interaction of SUR and Kir6.x with adenine nucleotides is an important issue to understand the molecular mechanisms underlying the metabolic regulation of the K-ATP channels. We analyzed direct interactions with adenine mucleotides of each subunit of K-ATP channels. Kir6.2 binds adenine nucleotides in a M2+-independent manner. SUR has two NBFs which are not equivalent: NBF1 is a Mg2+-independent high affinity nucleotide binding site, whereas NBF2 is a Mg-dependent low affinity site. Although SUR has ATPase activity at NBF2. it is not used to transport substrates against the concentration gradient unlike other ABC proteins. The ATPase cycle at NBF2 serves as a sensor of cellular metabolism. This may explain the low ATP hydrolysis rate compared to other ABC proteins. Based on studies of photoaffinity labeling, a model of K-ATP channel regulation is proposed, in which K-ATP channel activity is regulated by SUR via monitoring the intracellular M-ADP concentration. K channel activation is expected to be induced by the cooperative interaction of ATP ATP binding at NBF1 and MgADP binding at NBF2. (c) 2005 Elsevier Ltd. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.yjmcc.2004.11.021
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/15910875
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000229806700003&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.yjmcc.2004.11.021
  • ISSN : 0022-2828
  • eISSN : 1095-8584
  • PubMed ID : 15910875
  • Web of Science ID : WOS:000229806700003

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