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- W2146307680 abstract "Changes in cellular Ca2+ concentrations form a ubiquitous signal regulating numerous processes such as fertilization, differentiation, proliferation, contraction, and secretion. The Ca2+ signal, highly organized in space and time, is generated by the cellular Ca2+ signaling toolkit. Lysophospholipids, such as sphingosine-1-phosphate (S1P), sphingosylphosphorylcholine (SPC), or lysophosphatidic acid (LPA) use this toolkit in a specific manner to initiate their cellular responses. Acting as agonists at G protein-coupled receptors, S1P, SPC, and LPA increase the intracellular free Ca2+ concentration ([Ca2+]i) by using the classical, phospholipase C (PLC)-dependent pathway as well as PLC-independent pathways such as sphingosine kinase (SphK)/S1P. The S1P1 receptor, via protein kinase C, inhibits the [Ca2+]i transients caused by other receptors. Both S1P and SPC also act intracellularly to regulate [Ca2+]i. Intracellular S1P mobilizes Ca2+ in intact cells independently of G protein-coupled S1P receptors, and Ca2+ signaling by many agonists requires SphK-mediated S1P production. As shown for the FcεRI receptor, PLC and SphK may contribute specific components to the overall [Ca2+]i transient. Of the many open questions, identification of the intracellular S1P target site(s) appears to be of particular importance." @default.
- W2146307680 created "2016-06-24" @default.
- W2146307680 creator A5061649877 @default.
- W2146307680 date "2004-01-01" @default.
- W2146307680 modified "2023-10-14" @default.
- W2146307680 title "Lysophospholipid receptor-dependent and -independent calcium signaling" @default.
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- W2146307680 doi "https://doi.org/10.1002/jcb.20107" @default.
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