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• W1996890919 startingPage "979" @default.
• W1996890919 abstract "A large amount of data and observations on inositol 1,4,5-trisphosphate (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state activity of the channel, and its inactivation by IP(3) can be explained by assuming one activation and one inhibition module, both allosterically operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven by IP(3), Ca(2+), and the interconversion between two possible conformations of the receptor. The adaptation module becomes completely insensitive to a second IP(3) pulse within 80 s. Observed kinetic responses are well reproduced if, in addition, two module open states are rendered inactive by the current charge carrier Mn(2+). The inactivation time constants are 59 s in the activation, and 0.75 s in the adaptation module. The in vivo open probability of the channel is predicted to be almost in coincidence with the behavior in lipid bilayers for IP(3) levels of 0.2 and 2 microM and one-order-higher at 0.02 microM IP(3), whereas at 180 microM IP(3) the maximal in vivo activity may be 2.5-orders higher than in bilayers and restricted to a narrower Ca(2+) domain (approximately 10 microM-wide versus approximately 100 microM-wide). IP(3) is likely to inhibit channel activity at < or =120 nM Ca(2+) in vivo." @default.
• W1996890919 created "2016-06-24" @default.
• W1996890919 creator A5025604931 @default.
• W1996890919 date "2005-08-01" @default.
• W1996890919 modified "2023-10-11" @default.
• W1996890919 title "Gating Mechanisms of the Type-1 Inositol Trisphosphate Receptor" @default.
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• W1996890919 doi "https://doi.org/10.1529/biophysj.105.059238" @default.
• W1996890919 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1366646" @default.
• W1996890919 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15908571" @default.
• W1996890919 hasPublicationYear "2005" @default.
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