ArticleThe Journal of biological chemistry2007
The spatial distribution of inositol 1,4,5-trisphosphate receptor isoforms shapes Ca2+ waves.
Article in The Journal of biological chemistry, 2007. 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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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Stochastic model of IP3-induced Ca2+ spiking of HEK293 cells.PLoS computational biology · 2025Article
- Glucagon, cyclic AMP, and hepatic glucose mobilization: A half-century of uncertainty.Physiological reports · 2022Review
- IPiScience · 2020Article
- Spatial-temporal patterning of CaSeminars in cell & developmental biology · 2019Review
- Chronic alcohol feeding potentiates hormone-induced calcium signalling in hepatocytes.The Journal of physiology · 2017Article
- Hepatic Inositol 1,4,5 Trisphosphate Receptor Type 1 Mediates Fatty Liver.Hepatology communications · 2017Article
- The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Biochimica et biophysica acta · 2015Review
- Nuclear Factor, Erythroid 2-Like 2 Regulates Expression of Type 3 Inositol 1,4,5-Trisphosphate Receptor and Calcium Signaling in Cholangiocytes.Gastroenterology · 2015Article
- Apical localization of inositol 1,4,5-trisphosphate receptors is independent of extended synaptotagmins in hepatocytes.PloS one · 2014Article
- Altered responsiveness to extracellular ATP enhances acetaminophen hepatotoxicity.Cell communication and signaling : CCS · 2013Article
- Calcium signaling in the liver.Comprehensive Physiology · 2013Review
- Microdomains of muscarinic acetylcholine and Ins(1,4,5)P₃ receptors create 'Ins(1,4,5)P₃ junctions' and sites of Ca²+ wave initiation in smooth muscle.Journal of cell science · 2012Article
- Calcium-dependent physiologic and pathologic stimulus-metabolic response coupling in hepatocytes.Cell calcium · 2012Review
- Calcium signalling and liver regeneration.International journal of hepatology · 2012Article
- Article
- Inositol 1,4,5-trisphosphate receptor subtype-specific regulation of calcium oscillations.Neurochemical research · 2011Review
- The type I inositol 1,4,5-trisphosphate receptor interacts with protein 4.1N to mediate neurite formation through intracellular Ca waves.Neuro-Signals · 2011Article
- The type III inositol 1,4,5-trisphosphate receptor is associated with aggressiveness of colorectal carcinoma.Cell calcium · 2010Article
- IP(3)-dependent, post-tetanic calcium transients induced by electrostimulation of adult skeletal muscle fibers.The Journal of general physiology · 2010Article
- Regulation of multidrug resistance-associated protein 2 by calcium signaling in mouse liver.Hepatology (Baltimore, Md.) · 2010Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Cytosolic Ca(2+) is a versatile second messenger that can regulate multiple cellular processes simultaneously. This is accomplished in part through Ca(2+) waves and other spatial patterns of Ca(2+) signals. To investigate the mechanism responsible for the formation of Ca(2+) waves, we examined the role of inositol 1,4,5-trisphosphate receptor (InsP3R) isoforms in Ca(2+) wave formation. Ca(2+) signals were examined in hepatocytes, which express the type I and II InsP3R in a polarized fashion, and in AR4-2J cells, a nonpolarized cell line that expresses type I and II InsP3R in a ratio similar to what is found in hepatocytes but homogeneously throughout the cell. Expression of type I or II InsP3R was selectively suppressed by isoform-specific DNA antisense in an adenoviral delivery system, which was delivered to AR4-2J cells in culture and to hepatocytes in vivo. Loss of either isoform inhibited Ca(2+) signals to a similar extent in AR4-2J cells. In contrast, loss of the basolateral type I InsP3R decreased the sensitivity of hepatocytes to vasopressin but had little effect on the initiation or spread of Ca(2+) waves across hepatocytes. Loss of the apical type II isoform caused an even greater decrease in the sensitivity of hepatocytes to vasopressin and resulted in Ca(2+) waves that were much slower and delayed in onset. These findings provide evidence that the apical concentration of type II InsP3Rs is essential for the formation of Ca(2+) waves in hepatocytes. The subcellular distribution of InsP3R isoforms may critically determine the repertoire of spatial patterns of Ca(2+) signals.
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Registered trials
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