IP3 Receptor and Ca2+ Signaling
Calcium ions (Ca2+) are ubiquitous second messengers that play an important role in many physiological events including secretion, development, fertilization, and gene expression. However, the proper spatio-temporal regulation of the intracellular Ca2+ co
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IP3 Receptor and Ca2+ Signaling
C. Hisatsune . K. Mikoshiba
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Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 566
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Characters of Ca2+ Release from IP3Rs in Neurons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 567
3 3.1 3.2 3.3 3.4 3.5 3.6 3.7
Regulation of the IP3 Receptor by Various Associated Proteins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 569 Regulation of Subcellular IP3R Dynamics by 4.1N . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 569 Homer Activity dependently Controls the Coupling Status of mGluR–IP3R Signaling . . . . . . . . . . 570 Cytochrome c Accerelates Apoptosis by Increasing the Channel Activity of IP3Rs . . . . . . . . . . . . . . . . 571 Implication of IP3R-mediated Ca2+ Signaling in Huntington Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 571 Control of IP3Rs by Luminal IP3R-Binding Proteins, ERp44 and Chromogranins . . . . . . . . . . . . . . . . 572 ERp44 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 572 Chromogranin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 573
4 The Physiological Role of IP3R1 in the Brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574 4.1 Disturbed Motor Learning and Motor Coordination in the IP3R1 Mutant Mice . . . . . . . . . . . . . . . . 574 4.2 Abnormal Synaptic Plasticity in IP3R1-Deficient Mice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 574 5
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Concluding Remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 575
2009 Springer ScienceþBusiness Media, LLC.
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IP3 receptor and Ca2+ signaling
Abstract: Calcium ions (Ca2+) are ubiquitous second messengers that play an important role in many physiological events including secretion, development, fertilization, and gene expression. However, the proper spatio-temporal regulation of the intracellular Ca2+ concentration is necessary to fulfill the function, and disturbed Ca2+ signaling is known to cause cell death and pathological disease. Inositol 1, 4, 5-trisphosphate receptor (IP3R) is a Ca2+ channel localized on the endoplasmic reticulum (ER) in the many types of cells including neurons, and is a key player to generate the proper intracellular Ca2+ dynamics for cell function. Disruption of IP3Rs leads to various physiological defects including neural development and neural plasticity. Moreover, several lines of evidence indicate that the alte
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