ArticleProceedings of the National Academy of Sciences of the United States of America2001
Activation of calcium entry in human carcinoma A431 cells by store depletion and phospholipase C- dependent mechanisms converge on ICRAC-like calcium channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Patient-Specific iPSC-Based Models of Huntington's Disease as a Tool to Study Store-Operated Calcium Entry Drug Targeting.Frontiers in pharmacology · 2018Article
- UTP - Gated Signaling Pathways of 5-HT Release from BON Cells as a Model of Human Enterochromaffin Cells.Frontiers in pharmacology · 2017Article
- STIM1 and STIM2 proteins differently regulate endogenous store-operated channels in HEK293 cells.The Journal of biological chemistry · 2015Article
- STIM1 Protein Activates Store-Operated Calcium Channels in Cellular Model of Huntington's Disease.Acta naturae · 2014Article
- The uncoupling of synaptic protein homer 1c from target proteins activates store-operated calcium entry in a neurotransmitter-like manner in human neuroblastoma cells.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2013Article
- Regulation of store-operated channels by scaffold proteins in a431 cells.Acta naturae · 2010Article
- InsP3-mediated intracellular calcium signalling is altered by expression of synaptojanin-1.The Biochemical journal · 2004Article
- The store-operated calcium entry pathways in human carcinoma A431 cells: functional properties and activation mechanisms.The Journal of general physiology · 2003Article
- Activation of store-operated channels by noradrenaline via protein kinase C in rabbit portal vein myocytes.The Journal of physiology · 2002Article
- Transient receptor potential 1 regulates capacitative Ca(2+) entry and Ca(2+) release from endoplasmic reticulum in B lymphocytes.The Journal of experimental medicine · 2002Article
- Bilirubin binding to normal and modified human erythrocyte membranes: effect of phospholipases, neuraminidase, trypsin and CaCl2.Molecular and cellular biochemistry · 2001Article
- Human Trp3 forms both inositol trisphosphate receptor-dependent and receptor-independent store-operated cation channels in DT40 avian B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Delay in I(min) channel activation induced by dissociation of Homer proteins in A431 cells.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Activation of phospholipase C in nonexcitable cells causes the release of calcium (Ca2+) from intracellular stores and activation of Ca2+ influx by means of Ca2+ release-activated channels (ICRAC) in the plasma membrane. The molecular identity and the mechanism of ICRAC channel activation are poorly understood. Using the patch-clamp technique, here we describe the plasma membrane Ca2+ channels in human carcinoma A431 cells, which can be activated by extracellular UTP, by depletion of intracellular Ca2+ stores after exposure to the Ca2+-pump inhibitor thapsigargin, or by loading the cells with Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate. The observed channels display the same conductance and gating properties as previously described I(min) channels, but have significantly lower conductance for monovalent cations than the ICRAC channels. Thus, we concluded that the depletion-activated Ca2+ current in A431 cells is supported by I(CRAC)-like (ICRACL) channels, identical to I(min). We further demonstrated synergism in activation of ICRACL Ca2+ channels by extracellular UTP and intracellular inositol (1,4,5)-triphosphate (IP3), apparently because of reduction in phosphatidylinositol 4,5-bisphosphate (PIP2) levels in the patch. Prolonged exposure of patches to thapsigargin renders ICRACL Ca2+ channels unresponsive to IP3 but still available to activation by the combined action of IP3 and anti-PIP2 antibody. Based on these data, we concluded that phospholipase C-mediated and store-operated Ca2+ influx pathways in A431 cells converge on the same I(CRACL) Ca2+ channel, which can be modulated by PIP2.
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