Inositol Trisphosphate Receptor Ca2+ Release Channels
TL;DR: Over the last decade, detailed quantitative studies of InsP3R channel function and its regulation by ligands and interacting proteins have provided new insights into a remarkable richness of channel regulation and of the structural aspects that underlie signal transduction and permeation.
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Abstract: The inositol 1,4,5-trisphosphate (InsP3) receptors (InsP3Rs) are a family of Ca2+ release channels localized predominately in the endoplasmic reticulum of all cell types. They function to release Ca2+ into the cytoplasm in response to InsP3 produced by diverse stimuli, generating complex local and global Ca2+ signals that regulate numerous cell physiological processes ranging from gene transcription to secretion to learning and memory. The InsP3R is a calcium-selective cation channel whose gating is regulated not only by InsP3, but by other ligands as well, in particular cytoplasmic Ca2+. Over the last decade, detailed quantitative studies of InsP3R channel function and its regulation by ligands and interacting proteins have provided new insights into a remarkable richness of channel regulation and of the structural aspects that underlie signal transduction and permeation. Here, we focus on these developments and review and synthesize the literature regarding the structure and single-channel properties of the InsP3R.
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References
Structural analogues of D-myo-inositol-1,4,5-trisphosphate and adenophostin A: recognition by cerebellar and platelet inositol-1,4,5-trisphosphate receptors.
Christine T. Murphy,Andrew M. Riley,C. J. Lindley,David J. Jenkins,John Westwick,Barry V. L. Potter +5 more
TL;DR: This study is the first to demonstrate the activity of a synthetic disaccharide at the Ins(1, 4, 5)P3 receptor and that the Ins (1,4,5)P 3 receptor is capable of accommodating an increased steric bulk.
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Effect of mutation of a calmodulin binding site on Ca2+ regulation of inositol trisphosphate receptors.
Xianchao Zhang,Suresh K. Joseph +1 more
TL;DR: The data suggest that the CaM binding motif involving the W1577A locus does not play a role in Ca(2+) regulation of IP(3)R channel activity.
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The N-terminal Ca2+-independent calmodulin-binding site on the inositol 1,4,5-trisphosphate receptor is responsible for calmodulin inhibition, even though this inhibition requires Ca2+.
Nael Nadif Kasri,Geert Bultynck,Jeremy T. Smyth,Karolina Szlufcik,Jan B. Parys,Geert Callewaert,Ludwig Missiaen,Rafael A. Fissore,Katsuhiko Mikoshiba,Humbert De Smedt +9 more
TL;DR: It is concluded that CaM inhibits IICR via the N-terminal binding site of the Ca(2+)-independent CaM-binding site through the functional effect of CaM and induced an allosteric but competitive inhibition of IP(3) binding.
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Chapter 9 – structure and function of inositol trisphosphate receptors
Colin W. Taylor,Alan Richardson +1 more
- 01 Jan 1993
TL;DR: The intracellular receptor that mediates Ins(1,4,5)P3-stimulated Ca2+ mobilization has been purified and functionally reconstituted, and its amino acid sequence deduced from its cDNA sequence is demonstrated.
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Isoform dependent formation of heteromeric Ca2+ release channels (ryanodine receptors)
Bailong Xiao,Haruko Masumiya,Dawei Jiang,Ruiwu Wang,Yoshitatsu Sei,Lin Zhang,Takashi Murayama,Yasuo Ogawa,F. Anthony Lai,Terence Wagenknecht,S.R. Wayne Chen +10 more
TL;DR: Observations demonstrate that RyR2 is capable of forming functional heteromeric channels with RyR3 and RyR1, whereasRyR1 is incapable of forming heteromerics channels withRyR3.
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