Abstract
The interaction between Rab3A and calmodulin is necessary for the inhibitory effect of Rab3A in neuroendocrine cells. Contrastingly, Rab3A triggers the exocytosis known as acrosome reaction in permeabilized spermatozoa. Here we show that a Rab3A mutant that cannot bind calmodulin was fully capable of triggering acrosomal exocytosis. Additionally, calmodulin by itself abrogated the exocytosis triggered by Rab3A. The effect was observed with both the wild type protein and the calmodulin binding deficient mutant. Our results indicate that the inhibitory and stimulatory effects of Rab3A in different exocytic processes are mediated by different effectors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acrosome Reaction / drug effects
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Acrosome Reaction / physiology*
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Calcimycin / pharmacology
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Calmodulin / antagonists & inhibitors
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Calmodulin / metabolism*
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Calmodulin / pharmacology
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Cell Membrane Permeability
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Chlorpromazine / pharmacology
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Dopamine Antagonists / pharmacology
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Enzyme Inhibitors / pharmacology
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Exocytosis / drug effects
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Exocytosis / physiology*
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Fluorescent Dyes
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Humans
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Ionophores / pharmacology
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Male
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Mutation
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Progesterone / pharmacology
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Protein Binding / physiology
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Spermatozoa / cytology
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Spermatozoa / drug effects
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Spermatozoa / metabolism
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rab3A GTP-Binding Protein / genetics
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rab3A GTP-Binding Protein / metabolism*
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rab3A GTP-Binding Protein / pharmacology
Substances
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Calmodulin
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Dopamine Antagonists
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Enzyme Inhibitors
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Fluorescent Dyes
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Ionophores
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Calcimycin
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Progesterone
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rab3A GTP-Binding Protein
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Chlorpromazine