Abstract
Fertilization is accompanied by a transient increase in the concentration of intracellular Ca2+, which serves as a signal for initiating development. Some of the Ca2+ appears to be released from intracellular stores by the binding of inositol trisphosphate (IP3) to its receptor. However, in sea urchin eggs, other mechanisms appear to participate. Cyclic adenosine diphosphate--ribose (cADPR), a naturally occurring metabolite of nicotinamide adenine dinucleotide, is as potent as IP3 in mobilizing Ca2+ in sea urchin eggs. Experiments with antagonists of the cADPR and IP3 receptors revealed that both Ca2+ mobilizing systems were activated during fertilization. Blockage of either of the systems alone was not sufficient to prevent the sperm-induced Ca2+ transient. This study provides direct evidence for a physiological role of cADPR in the Ca2+ signaling process.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Diphosphate Ribose / analogs & derivatives
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Adenosine Diphosphate Ribose / pharmacology
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Animals
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Calcium / metabolism*
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Calcium Channels*
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Cyclic ADP-Ribose
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Cyclic AMP / analogs & derivatives
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Cyclic AMP / pharmacology
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Female
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Fertilization*
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Heparin / pharmacology
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Inositol 1,4,5-Trisphosphate / pharmacology
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Inositol 1,4,5-Trisphosphate Receptors
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Ovum / metabolism*
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Receptors, Cell Surface / physiology*
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Receptors, Cytoplasmic and Nuclear*
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Sea Urchins
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Signal Transduction
Substances
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Calcium Channels
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Inositol 1,4,5-Trisphosphate Receptors
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Receptors, Cell Surface
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Receptors, Cytoplasmic and Nuclear
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cyclic ADP-ribose receptor
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Cyclic ADP-Ribose
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8-aminoadenosine cyclic 3',5'-(hydrogen phosphate) 5'-ribofuranosyl ester
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Adenosine Diphosphate Ribose
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Inositol 1,4,5-Trisphosphate
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Heparin
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Cyclic AMP
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Calcium