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PubMed · 9812976

Ca2+ pool emptying stimulates Ca2+ entry activated by S-nitrosylation.

C J Favre·C A Ufret-Vincenty·M R Stone·H T Ma·D L Gill
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Abstract

The entry of Ca2+ following Ca2+ pool release is a major component of Ca2+ signals; yet despite intense study, how "store-operated" entry channels are activated is unresolved. Because S-nitrosylation has become recognized as an important regulatory modification of several key channel proteins, its role in Ca2+ entry was investigated. A novel class of lipophilic NO donors activated Ca2+ entry independent of the well defined NO target, guanylate cyclase. Strikingly similar entry of Ca2+ induced by cell permeant alkylators indicated that this Ca2+ entry process was activated through thiol modification. Significantly, Ca2+ entry activated by either NO donors or alkylators was highly stimulated by Ca2+ pool depletion, which increased both the rate of Ca2+ release and the sensitivity to thiol modifiers. The results indicate that S-nitrosylation underlies activation of an important store-operated Ca2+ entry mechanism.

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Alkylating AgentsAnimalsBiological TransportCalciumCalcium SignalingCells, CulturedCricetinaeLungMuscle, SmoothNitric OxideNitritesNitroprussideNitroso CompoundsSulfhydryl CompoundsTriazolesJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.

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C J Favre, C A Ufret-Vincenty, M R Stone, H T Ma, D L Gill. 1998-11-20. Ca2+ pool emptying stimulates Ca2+ entry activated by S-nitrosylation.. https://doi.org/10.1074/jbc.273.47.30855

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