ArticleThe Journal of physiology2004
Fast Ca(2+)-dependent inactivation of the store-operated Ca2+ current (ISOC) in liver cells: a role for calmodulin.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Mutations in proteins involved in E-C coupling and SOCE and congenital myopathies.The Journal of general physiology · 2022Review
- Highlighting the Multifaceted Role of Orai1 N-Terminal- and Loop Regions for Proper CRAC Channel Functions.Cells · 2022Review
- Fumaric Acids Do Not Directly Influence Gene Expression of Neuroprotective Factors in Highly Purified Rodent Astrocytes.Brain sciences · 2019Article
- Molecular physiology and pathophysiology of stromal interaction molecules.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Calmodulin dissociates the STIM1-Orai1 complex and STIM1 oligomers.Nature communications · 2017Article
- HMGB1 release by HCell death discovery · 2017Article
- Molecular mechanisms of STIM/Orai communication.American journal of physiology. Cell physiology · 2016Review
- 5-Aminoimidazole-4-carboxyamide-1-β-D-ribofranoside stimulates the rat enhancer of split- and hairy-related protein-2 gene via atypical protein kinase C lambda.Journal of biochemistry · 2016Article
- Orai1 pore residues control CRAC channel inactivation independently of calmodulin.The Journal of general physiology · 2016Article
- Store-Operated Calcium Channels.Physiological reviews · 2015Review
- Structural and functional mechanisms of CRAC channel regulation.Journal of molecular biology · 2015Review
- Dynamic assembly of a membrane signaling complex enables selective activation of NFAT by Orai1.Current biology : CB · 2014Article
- The serine-threonine phosphatase calcineurin is a regulator of endothelial store-operated calcium entry.Pulmonary circulation · 2014Article
- TRPM2 channels mediate acetaminophen-induced liver damage.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Calcium-regulation of mitochondrial respiration maintains ATP homeostasis and requires ARALAR/AGC1-malate aspartate shuttle in intact cortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- STIM proteins: dynamic calcium signal transducers.Nature reviews. Molecular cell biology · 2012Review
- Permeation, selectivity and gating in store-operated CRAC channels.The Journal of physiology · 2012Review
- Effects and mechanisms of store-operated calcium channel blockade on hepatic ischemia-reperfusion injury in rats.World journal of gastroenterology · 2012Article
- Orai3--the 'exceptional' Orai?The Journal of physiology · 2012Review
- Store-operated calcium channels: new perspectives on mechanism and function.Cold Spring Harbor perspectives in biology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Store-operated Ca2+ channels (SOCs) provide a major pathway for Ca2+ entry in non-excitable cells. SOCs in immortalized liver cells are highly selective for Ca2+ over other cations and are similar to well-studied Ca2+ release activated Ca2+ (CRAC) channels in haematopoietic cell lines. In the present work, employing H4IIE liver cells, we investigated fast inactivation of SOC current (ISOC), which occurs at membrane potentials below -60 mV. This inactivation was significantly reduced when BAPTA, a faster Ca2+ buffer, was used instead of EGTA, and was completely abolished if Na+ was used as a charge carrier in the absence of divalent cations in the external medium. These results suggested that fast inactivation of SOCs in H4IIE cells was Ca2+ dependent and was similar to the fast inactivation of CRAC channels. Experiments showing that the fast inactivation of ISOC was not affected by the disruption of actin by latrunculin B indicate that the cytoskeleton is unlikely to be involved. To elucidate the mechanism of Ca2+ dependence, a possible role of calmodulin (CaM) in SOCs' fast inactivation was investigated. The CaM inhibitors Mas-7 and calmidazolium failed to affect ISOC fast inactivation, whereas over-expression of a CaM inhibitor peptide or a mutant CaM lacking functional EF hands significantly altered the inactivation of ISOC. Out of two exponential components normally required to approximate kinetics of ISOC fast inactivation, the faster component was reduced in amplitude by 30%, compared to the control. The results presented suggest that CaM is responsible for at least part of Ca(2+)-dependent fast inactivation of ISOC in liver cells. It is hypothesized that CaM is tethered to the channel itself and therefore protected from chemical inhibitors.
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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.