ArticleThe Journal of biological chemistry2009
ATP regulation of type-1 inositol 1,4,5-trisphosphate receptor activity does not require walker A-type ATP-binding motifs.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
The trial behind it
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Cryo-EM insights into isoform-specific properties of the IPNature communications · 2026Article
- Conformational landscape and ligand-dependent clustering of the human type 2 IPNature communications · 2026Article
- Conformational landscape and clustering of human type 2 IPbioRxiv : the preprint server for biology · 2026Article
- Conformational motions and ligand-binding underlying gating and regulation in IPNature communications · 2022Article
- Functional determination of calcium-binding sites required for the activation of inositol 1,4,5-trisphosphate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- GPR40 activation initiates store-operated CaScientific reports · 2019Article
- Cryo-EM reveals ligand induced allostery underlying InsPCell research · 2018Article
- Region-specific proteolysis differentially regulates type 1 inositol 1,4,5-trisphosphate receptor activity.The Journal of biological chemistry · 2017Article
- Cardiac inositol 1,4,5-trisphosphate receptors.Biochimica et biophysica acta. Molecular cell research · 2017Review
- Ryanodine receptor resolution revolution: Implications for InsPCell calcium · 2017Article
- The trans-membrane domain of Bcl-2α, but not its hydrophobic cleft, is a critical determinant for efficient IP3 receptor inhibition.Oncotarget · 2016Article
- Unique Regulatory Properties of Heterotetrameric Inositol 1,4,5-Trisphosphate Receptors Revealed by Studying Concatenated Receptor Constructs.The Journal of biological chemistry · 2016Article
- The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Biochimica et biophysica acta · 2015Review
- Regulatory Mechanisms of Endoplasmic Reticulum Resident IP3 Receptors.Journal of molecular neuroscience : MN · 2015Review
- Inositol 1,4,5-trisphosphate receptors in the endoplasmic reticulum: A single-channel point of view.Cell calcium · 2015Review
- Using concatenated subunits to investigate the functional consequences of heterotetrameric inositol 1,4,5-trisphosphate receptors.Biochemical Society transactions · 2015Review
- Interactions of antagonists with subtypes of inositol 1,4,5-trisphosphate (IP3) receptor.British journal of pharmacology · 2014Article
- Functional inositol 1,4,5-trisphosphate receptors assembled from concatenated homo- and heteromeric subunits.The Journal of biological chemistry · 2013Article
- Patch-clamp electrophysiology of intracellular Ca2+ channels.Cold Spring Harbor protocols · 2013Article
- Fragmented inositol 1,4,5-trisphosphate receptors retain tetrameric architecture and form functional Ca2+ release channels.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
ATP is known to increase the activity of the type-1 inositol 1,4,5-trisphosphate receptor (InsP3R1). This effect is attributed to the binding of ATP to glycine rich Walker A-type motifs present in the regulatory domain of the receptor. Only two such motifs are present in neuronal S2+ splice variant of InsP3R1 and are designated the ATPA and ATPB sites. The ATPA site is unique to InsP3R1, and the ATPB site is conserved among all three InsP3R isoforms. Despite the fact that both the ATPA and ATPB sites are known to bind ATP, the relative contribution of these two sites to the enhancing effects of ATP on InsP3R1 function is not known. We report here a mutational analysis of the ATPA and ATPB sites and conclude neither of these sites is required for ATP modulation of InsP3R1. ATP augmented InsP3-induced Ca2+ release from permeabilized cells expressing wild type and ATP-binding site-deficient InsP3R1. Similarly, ATP increased the single channel open probability of the mutated InsP3R1 to the same extent as wild type. ATP likely exerts its effects on InsP3R1 channel function via a novel and as yet unidentified mechanism.
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Registered trials
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.