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pubmed-article:15223153pubmed:abstractTextIn various cell types cytosolic calcium (Ca(2+)) is an important regulator. The possible role of Ca(2+) release from the inositol 1,4,5-trisphosphate (IP(3)) receptor channel in the regulation of the phosphorylation-dephosphorylation cycle process involved in glycogen degradation by glycogen phosphorylase have theoretically investigated by using the Li-Rinzel model for cytosolic Ca(2+) oscillations. For the case of deterministic cytosolic Ca(2+) oscillations, there exists an optimal frequency of cytosolic Ca(2+) oscillations at which the average fraction of active glycogen phosphorylase reaches a maximum value, and a mutation for the average fraction of active glycogen phosphorylase occurs at the higher bifurcation point of Ca(2+) oscillations. For the case of stochastic cytosolic Ca(2+) oscillations, the fraction of active phosphorylase is strongly affected by the number of IP(3) receptor channels and the level of IP(3) concentration. Small number of IP(3) receptor channels can potentiate the sensitivity of the activity of glycogen phosphorylase. The average frequency and amplitude of active phosphorylase stochastic oscillations are increased with the level of increasing IP(3) stimuli. The various distributions for the amplitude of active glycogen phosphorylase oscillations in parameters plane are discussed.lld:pubmed
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pubmed-article:15223153pubmed:pagination179-90lld:pubmed
pubmed-article:15223153pubmed:dateRevised2007-7-18lld:pubmed
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pubmed-article:15223153pubmed:year2004lld:pubmed
pubmed-article:15223153pubmed:articleTitleEffects of inositol 1,4,5-trisphosphate receptor-mediated intracellular stochastic calcium oscillations on activation of glycogen phosphorylase.lld:pubmed
pubmed-article:15223153pubmed:affiliationDepartment of Physics, Central China Normal University, Wuhan 430079, Hubei, PR China. wud@phy.ccnu.edu.cnlld:pubmed
pubmed-article:15223153pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15223153pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed