ArticleProceedings of the National Academy of Sciences of the United States of America2002
Identification of a family of calcium sensors as protein ligands of inositol trisphosphate receptor Ca(2+) release channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.
- Calcium and arrhythmogenesis.Physiological reviews · 2007Pooled it
- Molecular basis for a CaThe Journal of biological chemistry · 2026Article
- Calmodulinopathy variants impair CaV1.3 and CaV2.1 regulation.The Journal of general physiology · 2026Article
- Structure-Function Diversity of Calcium-Binding Proteins (CaBPs): Key Roles in Cell Signalling and Disease.Cells · 2025Review
- Comprehensive Characterization of a Subfamily of CaeNeuro · 2024Article
- Calcium-Associated Proteins in Neuroregeneration.Biomolecules · 2024Review
- Complicity of α-synuclein oligomer and calcium dyshomeostasis in selective neuronal vulnerability in Lewy body disease.Archives of pharmacal research · 2021Review
- Lessons from the Endoplasmic Reticulum CaCells · 2020Review
- Characterization of NCS1-InsP3R1 interaction and its functional significance.The Journal of biological chemistry · 2019Article
- α-Synuclein oligomers mediate the aberrant form of spike-induced calcium release from IPScientific reports · 2019Article
- Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019Review
- Structure and Function of IPCold Spring Harbor perspectives in biology · 2019Review
- InsPBMC biology · 2018Article
- RCN1 suppresses ER stress-induced apoptosis via calcium homeostasis and PERK-CHOP signaling.Oncogenesis · 2017Article
- CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Maintenance of normal blood pressure is dependent on IP3R1-mediated regulation of eNOS.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Inositol 1,4,5-trisphosphate receptors and their protein partners as signalling hubs.The Journal of physiology · 2016Review
- Article
- Sense and specificity in neuronal calcium signalling.Biochimica et biophysica acta · 2015Review
- ¹H, ¹⁵N, and ¹³C chemical shift assignments of murine calcium-binding protein 4.Biomolecular NMR assignments · 2014Article
19 more citing papers are in PubMed but not listed here.
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7 authors at 2 institutions in 1 country.
Funding
Abstract
The inositol trisphosphate (InsP(3)) receptor (InsP(3)R) is a ubiquitously expressed intracellular Ca(2+) channel that mediates complex cytoplasmic Ca(2+) signals, regulating diverse cellular processes, including synaptic plasticity. Activation of the InsP(3)R channel is normally thought to require binding of InsP(3) derived from receptor-mediated activation of phosphatidylinositol lipid hydrolysis. Here we identify a family of neuronal Ca(2+)-binding proteins as high-affinity protein agonists of the InsP(3)R, which bind to the channel and activate gating in the absence of InsP(3). CaBP/caldendrin, a subfamily of the EF-hand-containing neuronal calcium sensor family of calmodulin-related proteins, bind specifically to the InsP(3)-binding region of all three InsP(3)R channel isoforms with high affinity (K(a) approximately 25 nM) in a Ca(2+)-dependent manner (K(a) approximately 1 microM). Binding activates single-channel gating as efficaciously as InsP(3), dependent on functional EF-hands in CaBP. In contrast, calmodulin neither bound with high affinity nor activated channel gating. CaBP1 and the type 1 InsP(3)R associate in rat whole brain and cerebellum lysates, and colocalize extensively in subcellular regions in cerebellar Purkinje neurons. Thus, InsP(3)R-mediated Ca(2+) signaling in cells is possible even in the absence of InsP(3) generation, a process that may be particularly important in responding to and shaping changes in intracellular Ca(2+) concentration by InsP(3)-independent pathways and for localizing InsP(3)-mediated Ca(2+) signals to individual synapses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.