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ECB-ART-36346
Biochem J 1996 Jun 15;316 ( Pt 3):709-11. doi: 10.1042/bj3160709.
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Nicotinate-adenine dinucleotide phosphate-induced Ca(2+)-release does not behave as a Ca(2+)-induced Ca(2+)-release system.

Chini EN , Dousa TP .


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We investigated the dependence of nicotinate-adenine dinucleotide phosphate (NAADP)-induced Ca2+ release from intracellular stores of sea urchin egg homogenates, upon extravesicular Ca2+. In contrast to the Ca2+ release induced inositol 1'',4'',5''-triphosphate (IP3) or cyclic ADP-ribose (cADPR), the Ca2+ release induced by NAADP was completely independent of the free extravesicular Ca2+ over a wide range of concentrations (0-0.1 mM). The Ca2+ release triggered by either cADPR or IP3 was biphasically modulated by extravesicular Ca2+, and the Ca2+ release by these agents was abolished when the extravesicular Ca2+ was removed by chelation with 2 mM EGTA. On the other hand, NAADP-triggered Ca2+ release was not influenced by EGTA. These data indicate that while both cADPR and IP3 systems behave as functional Ca(2+)-induced Ca2+ release mechanisms, NAADP activates a Ca2+ release mechanism which is independent of the presence of extravesicular Ca2+. Therefore, the NAADP-sensitive Ca2+ release mechanisms may have a unique regulatory impact upon intracellular Ca2+ homoeostasis.

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Genes referenced: impact LOC100887844 srpl

References [+] :
Berridge, The biology and medicine of calcium signalling. 1994, Pubmed