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Lysophospholipid receptor‐dependent and ‐independent calcium signaling
Author(s) -
Meyer zu Heringdorf Dagmar
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20107
Subject(s) - lysophosphatidic acid , sphingosine 1 phosphate , sphingosine , microbiology and biotechnology , sphingosine kinase , g protein coupled receptor , receptor , signal transduction , intracellular , lipid signaling , phospholipase c , calcium signaling , protein kinase c , biology , gq alpha subunit , chemistry , biochemistry
Changes in cellular Ca 2+ concentrations form a ubiquitous signal regulating numerous processes such as fertilization, differentiation, proliferation, contraction, and secretion. The Ca 2+ signal, highly organized in space and time, is generated by the cellular Ca 2+ 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 Ca 2+ concentration ([Ca 2+ ] i ) by using the classical, phospholipase C (PLC)‐dependent pathway as well as PLC‐independent pathways such as sphingosine kinase (SphK)/S1P. The S1P 1 receptor, via protein kinase C, inhibits the [Ca 2+ ] i transients caused by other receptors. Both S1P and SPC also act intracellularly to regulate [Ca 2+ ] i . Intracellular S1P mobilizes Ca 2+ in intact cells independently of G protein‐coupled S1P receptors, and Ca 2+ 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 [Ca 2+ ] i transient. Of the many open questions, identification of the intracellular S1P target site(s) appears to be of particular importance.