ArticleThe Journal of biological chemistry2008
The type 2 inositol (1,4,5)-trisphosphate (InsP3) receptor determines the sensitivity of InsP3-induced Ca2+ release to ATP in pancreatic acinar cells.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Cryo-EM insights into isoform-specific properties of the IPNature communications · 2026Article
- The Protective Effect of Nimodipine in Schwann Cells Is Related to the Upregulation of LMO4 and SERCA3 Accompanied by the Fine-Tuning of Intracellular Calcium Levels.International journal of molecular sciences · 2025Article
- Histamine-induced cytosolic calcium mobilization in human bronchial smooth muscle cells.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2025Article
- Conformational motions and ligand-binding underlying gating and regulation in IPNature communications · 2022Article
- Research Progress on the Relationship Between Acute Pancreatitis and Calcium Overload in Acinar Cells.Digestive diseases and sciences · 2019Review
- Inositol 1,4,5-Trisphosphate Receptors in Hypertension.Frontiers in physiology · 2018Review
- Hydrogen peroxide attenuates refilling of intracellular calcium store in mouse pancreatic acinar cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- 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
- Using concatenated subunits to investigate the functional consequences of heterotetrameric inositol 1,4,5-trisphosphate receptors.Biochemical Society transactions · 2015Review
- Role of vesicular nucleotide transporter VNUT (SLC17A9) in release of ATP from AR42J cells and mouse pancreatic acinar cells.Purinergic signalling · 2014Article
- Functional inositol 1,4,5-trisphosphate receptors assembled from concatenated homo- and heteromeric subunits.The Journal of biological chemistry · 2013Article
- IP3R2 levels dictate the apoptotic sensitivity of diffuse large B-cell lymphoma cells to an IP3R-derived peptide targeting the BH4 domain of Bcl-2.Cell death & disease · 2013Article
- Differential regulation of the InsP₃ receptor type-1 and -2 single channel properties by InsP₃, Ca²⁺ and ATP.The Journal of physiology · 2012Article
- Article
- Regulation of Ca²⁺ release through inositol 1,4,5-trisphosphate receptors by adenine nucleotides in parotid acinar cells.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Ca-induced Ca Release from Internal Stores in INS-1 Rat Insulinoma Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Pancreatic acinar cells: molecular insight from studies of signal-transduction using transgenic animals.The international journal of biochemistry & cell biology · 2010Review
- Linking structure to function: Recent lessons from inositol 1,4,5-trisphosphate receptor mutagenesis.Cell calcium · 2010Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Calcium release through inositol (1,4,5)-trisphosphate receptors (InsP(3)R) is the primary signal driving digestive enzyme and fluid secretion from pancreatic acinar cells. The type 2 (InsP(3)R2) and type 3 (InsP(3)R3) InsP(3)R are the predominant isoforms expressed in acinar cells and are required for proper exocrine gland function. Both InsP(3)R2 and InsP(3)R3 are positively regulated by cytosolic ATP, but InsP(3)R2 is 10-fold more sensitive than InsP(3)R3 to this form of modulation. In this study, we examined the role of InsP(3)R2 in setting the sensitivity of InsP(3)-induced Ca(2+) release (IICR) to ATP in pancreatic acinar cells. IICR was measured in permeabilized acinar cells from wild-type (WT) and InsP(3)R2 knock-out (KO) mice. ATP augmented IICR from WT pancreatic cells with an EC(50) of 38 microm. However, the EC(50) was 10-fold higher in acinar cells isolated from InsP(3)R2-KO mice, indicating a role for InsP(3)R2 in setting the sensitivity of IICR to ATP. Consistent with this idea, heterologous expression of InsP(3)R2 in RinM5F cells, which natively express predominately InsP(3)R3, increased the sensitivity of IICR to ATP. Depletion of ATP attenuated agonist-induced Ca(2+) signaling in WT pancreatic acinar cells. This effect was more profound in acinar cells prepared from InsP(3)R2-KO mice. These data suggest that the sensitivity of IICR to ATP depletion is regulated by the particular complement of InsP(3)R expressed in an individual cell. The effects of metabolic stress on intracellular Ca(2+) signals can therefore be determined by the relative amount of InsP(3)R2 expressed in cells.
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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.