Contractile dysfunctions in ATP-dependent K+ channel-deficient mouse muscle during fatigue involve excessive depolarization and Ca2+ influx through L-type Ca2+ channels

scientific article published on 27 June 2008

Contractile dysfunctions in ATP-dependent K+ channel-deficient mouse muscle during fatigue involve excessive depolarization and Ca2+ influx through L-type Ca2+ channels is …
instance of (P31):
scholarly articleQ13442814

External links are
P356DOI10.1113/EXPPHYSIOL.2008.042572
P698PubMed publication ID18586858
P5875ResearchGate publication ID5268805

P2093author name stringBing Gong
Jean-Marc Renaud
Carlo Cifelli
Louise Boudreault
Jean-Philippe Bercier
P433issue10
P304page(s)1126-1138
P577publication date2008-06-27
P1433published inExperimental PhysiologyQ1091760
P1476titleContractile dysfunctions in ATP-dependent K+ channel-deficient mouse muscle during fatigue involve excessive depolarization and Ca2+ influx through L-type Ca2+ channels
P478volume93

Reverse relations

cites work (P2860)
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Q37894285Compartmentation of membrane processes and nucleotide dynamics in diffusion-restricted cardiac cell microenvironment
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Q33906965Human K(ATP) channelopathies: diseases of metabolic homeostasis
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Q41630359KATP channel deficiency in mouse FDB causes an impairment of energy metabolism during fatigue
Q35076166Muscle KATPChannels: Recent Insights to Energy Sensing and Myoprotection
Q41955529Potassium dependent rescue of a myopathy with core-like structures in mouse
Q35178696Properties of single FDB fibers following a collagenase digestion for studying contractility, fatigue, and pCa-sarcomere shortening relationship
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Q39893105Sarcolemmal ATP-sensitive K(+) channels control energy expenditure determining body weight
Q37417938Sarcolemmal ATP-sensitive potassium channels modulate skeletal muscle function under low-intensity workloads.

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