| http://purl.uniprot.org/citations/22357870 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22357870 | http://www.w3.org/2000/01/rdf-schema#comment | "Complexins are small soluble proteins that bind to assembling SNARE complexes during synaptic vesicle exocytosis, which in turn mediates neurotransmitter release. Complexins are required for clamping of spontaneous "mini " release and for the priming and synaptotagmin-dependent Ca(2+) triggering of evoked release. Mammalian genomes encode four complexins that are composed of an N-terminal unstructured sequence that activates synaptic exocytosis, an accessory α-helix that clamps exocytosis, an essential central α-helix that binds to assembling SNARE complexes and is required for all of its functions, and a long, apparently unstructured C-terminal sequence whose function remains unclear. Here, we used cultured mouse neurons to show that the C-terminal sequence of complexin-1 is not required for its synaptotagmin-activating function but is essential for its priming and clamping functions. Wild-type complexin-3 did not clamp exocytosis but nevertheless fully primed and activated exocytosis. Strikingly, exchanging the complexin-1 C terminus for the complexin-3 C terminus abrogated clamping, whereas exchanging the complexin-3 C terminus for the complexin-1 C terminus enabled clamping. Analysis of point mutations in the complexin-1 C terminus identified two single amino-acid substitutions that impaired clamping without altering the activation function of complexin-1. Examination of release induced by stimulus trains revealed that clamping-deficient C-terminal complexin mutants produced a modest relative increase in delayed release. Overall, our results show that the relatively large C-terminal complexin-1 sequence acts in priming and clamping synaptic exocytosis and demonstrate that the clamping function is not conserved in complexin-3, presumably because of its distinct C-terminal sequences."xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.org/dc/terms/identifier | "doi:10.1523/jneurosci.3360-11.2012"xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/author | "Yang X."xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/author | "Sudhof T.C."xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/author | "Kaeser-Woo Y.J."xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/name | "J Neurosci"xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/pages | "2877-2885"xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/title | "C-terminal complexin sequence is selectively required for clamping and priming but not for Ca2+ triggering of synaptic exocytosis."xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://purl.uniprot.org/core/volume | "32"xsd:string |
| http://purl.uniprot.org/citations/22357870 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22357870 |
| http://purl.uniprot.org/citations/22357870 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22357870 |
| http://purl.uniprot.org/uniprot/#_P63040-mappedCitation-22357870 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22357870 |
| http://purl.uniprot.org/uniprot/P63040 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/22357870 |