ArticleProceedings of the National Academy of Sciences of the United States of America1997
Distinct roles of C2A and C2B domains of synaptotagmin in the regulation of exocytosis in adrenal chromaffin cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 64 citations in OpenAlex.
- Synaptotagmin IV acts as a multi-functional regulator of Ca2+-dependent exocytosis.Neurochemical research · 2011Review
- Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- RNA interference-mediated silencing of synaptotagmin IX, but not synaptotagmin I, inhibits dense-core vesicle exocytosis in PC12 cells.The Biochemical journal · 2004Article
- Regulated exocytosis of an H+/myo-inositol symporter at synapses and growth cones.The EMBO journal · 2004Article
- The C2A domain of synaptotagmin-like protein 3 (Slp3) is an atypical calcium-dependent phospholipid-binding machine: comparison with the C2A domain of synaptotagmin I.The Biochemical journal · 2002Article
- Identification of a mammalian H(+)-myo-inositol symporter expressed predominantly in the brain.The EMBO journal · 2001Article
- Characterization of KIAA1427 protein as an atypical synaptotagmin (Syt XIII).The Biochemical journal · 2001Article
- Role of the conserved WHXL motif in the C terminus of synaptotagmin in synaptic vesicle docking.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Is double C2 protein (DOC2) expressed in bovine adrenal medulla? A commercial anti-DOC2 monoclonal antibody recognizes a major bovine mitochondrial antigen.The Biochemical journal · 2000Article
- The use of permeabilized cells to assay protein phosphorylation and catecholamine release.Neurochemical research · 2000Review
- Rapid regulated dense-core vesicle exocytosis requires the CAPS protein.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Synaptotagmin VII regulates Ca(2+)-dependent exocytosis of lysosomes in fibroblasts.The Journal of cell biology · 2000Article
- Functional and biochemical analysis of the C2 domains of synaptotagmin IV.Molecular biology of the cell · 1999Article
- Protein kinase C controls the priming step of regulated exocytosis in adrenal chromaffin cells.Cellular and molecular neurobiology · 1998Article
- Functional analysis of the C2A domain of synaptotagmin 1: implications for calcium-regulated secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- The first C2 domain of synaptotagmin is required for exocytosis of insulin from pancreatic beta-cells: action of synaptotagmin at low micromolar calcium.The EMBO journal · 1997Article
- Regulation by bivalent cations of phospholipid binding to the C2A domain of synaptotagmin III.The Biochemical journal · 1997Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptotagmin that contains two repeats of C2 regulatory domains is considered to be involved in neurotransmitter release. To reveal the roles of synaptotagmin in the regulation of exocytosis, we examined the effects of antibodies against C2A and C2B domains on Ca2+-evoked catecholamine (CA) release from digitonin-permeabilized adrenal chromaffin cells, resolving the Ca2+-evoked release into ATP-dependent priming and ATP-independent Ca2+-triggered steps. Anti-C2A antibody clearly reduced the ATP-independent release, suggesting that the C2A domain directly facilitate or promote Ca2+-triggered step, vesicular fusion. In contrast, anti-C2B antibody did not affect Ca2+-evoked release by itself, but significantly increased the spontaneous Ca2+-independent release. In addition, inositol high-polyphosphate series (IHPS) that bind the C2B domain inhibited both the ATP-independent Ca2+-evoked release and the spontaneous release in a dose-dependent manner. The inhibition by IHPS was totally reversed by anti-C2B antibody and significantly reversed by high concentration of Ca2+. These results suggest that IHPS binding to C2B domain arrests membrane fusion by presumably preventing interaction of synaptotagmin with phospholipids or with proteins of plasma membrane. Thus, IHPS binding to the C2B domain might keep the docked or primed vesicles away from spontaneous fusion at resting level of intracellular Ca2+. Binding of the increased intracellular Ca2+ to the C2A domain may facilitate or trigger the vesicular fusion by releasing this suppression by IHPS.
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