ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Functional analysis of the C2A domain of synaptotagmin 1: implications for calcium-regulated secretion.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 39 citations in OpenAlex.
- Polybasic Patches in Both C2 Domains of Synaptotagmin-1 Are Required for Evoked Neurotransmitter Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Risk of false positive genetic associations in complex traits with underlying population structure: a case study.Veterinary journal (London, England : 1997) · 2014Article
- Complexin arrests a pool of docked vesicles for fast Ca2+-dependent release.The EMBO journal · 2012Article
- Ion selectivities of the Ca(2+) sensors for exocytosis in rat phaeochromocytoma cells.The Journal of physiology · 2001Article
- The Exocytosis-regulatory protein synaptotagmin VII mediates cell invasion by Trypanosoma cruzi.The Journal of experimental medicine · 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
- alpha-Latrotoxin releases calcium in frog motor nerve terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Proteins involved in synaptic vesicle trafficking.The Journal of physiology · 1999Review
- Functional and biochemical analysis of the C2 domains of synaptotagmin IV.Molecular biology of the cell · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Synaptotagmin 1 is proposed to function as a low affinity calcium sensor for calcium-triggered exocytosis from neural and neuroendocrine cells. Because of the calcium-binding properties of the C2A domain of synaptotagmin 1, calcium-dependent interactions through this domain may modulate neurotransmitter release. We addressed this question by using alanine-scanning mutagenesis to generate a series of mutations within the C2A domain of synaptotagmin 1. The effects of these mutations on synaptotagmin 1 C2A function were analyzed for (1) calcium-dependent phospholipid binding, (2) calcium-dependent binding to syntaxin 1A, a plasma membrane protein critical for vesicle docking or fusion, and (3) calcium-regulated secretion after microinjection into neuroendocrine pheochromocytoma (PC12) cells. Our analyses reveal that a polylysine motif at residues 189-192 confers an inhibitory effect on secretion by recombinant synaptotagmin C2A fragments. The synaptotagmin 1 C2A polylysine motif functions independently of calcium-mediated interactions with phospholipids and syntaxin 1A. Furthermore, alpha-latrotoxin reverses the inhibitory effect of injected recombinant C2A fragments, suggesting that they perturb the cellular calcium-sensing machinery by interfering with synaptotagmin 1 activity in vivo. Our results indicate that novel calcium-independent interactions mediated through the C2A polylysine motif of synaptotagmin 1 function to modulate neurotransmitter release.
Indexed as
Identifiers
9570782PMC6793152W2100688616What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.