Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 275, Issue 12, Pages 8301-8306Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.275.12.8301
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- Telethon [963] Funding Source: Medline
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An intracellular mechanism activated by nicotinic acid adenine dinucleotide phosphate (NAADP(+)) contributes to intracellular Ca2+ release alongside inositol 1,4,5-trisphosphate (Ins-P-3) and ryanodine receptors. The NAADP(+)-sensitive mechanism has been shown to be operative in sea urchin eggs, ascidian eggs, and pancreatic acinar cells. Furthermore, most mammalian cell types can synthesize NAADP(+), with nicotinic acid and NADP(+) as precursors. In this contribution, NAADP(+) induced Ca2+ release has been investigated in starfish oocytes. Uncaging of injected NAADP(+) induced Ca2+ mobilization in both immature oocytes and in oocytes matured by the hormone 1-methyladenine (1-MA), The role of extracellular Ca2+ in NAADP(+)-induced Ca2+ mobilization, which was minor in immature oocytes, was instead essential in mature oocytes, Thus, the NAADP(+)-sensitive Ca2+ pool, which is known to be distinct from those sensitive to inositol 1,4,5-trisphosphate or cyclic ADPribose, apparently migrated closer to (or became part of) the plasma membrane during the maturation process. Inhibition of both Ins-P-3 and ryanodine receptors, but not of either alone, substantially inhibited NAADP(+)-induced Ca2+ mobilization in both immature and mature oocytes. The data also suggest that NAADP(+)-induced Ca2+ mobilization acted as a trigger for Ca2+ release via Ins-P-3 and ryanodine receptors.
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