| http://purl.uniprot.org/citations/12547917 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12547917 | http://www.w3.org/2000/01/rdf-schema#comment | "Mints (also called X11-like proteins) are adaptor proteins composed of divergent N-terminal sequences that bind to synaptic proteins such as CASK (Mint 1 only) and Munc18-1 (Mints 1 and 2) and conserved C-terminal PTB- and PDZ-domains that bind to widely distributed proteins such as APP, presenilins, and Ca(2+) channels (all Mints). We find that Mints 1 and 2 are similarly expressed in most neurons except for inhibitory interneurons that contain selectively high levels of Mint 1. Using knockout mice, we show that deletion of Mint 1 does not impair survival or alter the overall brain architecture, arguing against an essential developmental function of the Mint 1-CASK complex. In electrophysiological recordings in the hippocampus, we observed no changes in short- or long-term synaptic plasticity in excitatory synapses from Mint 1-deficient mice and detected no alterations in the ratio of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) to N-methyl-d-aspartate (NMDA) receptor-mediated synaptic currents. Thus the Mint 1-CASK complex is not required for AMPA- and NMDA-receptor functions or for synaptic plasticity in excitatory synapses. In inhibitory synapses, however, we uncovered an approximately 3-fold increase in presynaptic paired-pulse depression, suggesting that deletion of Mint 1 impairs the regulation of gamma-aminobutyric acid release. Our data indicate that Mints 1 and 2 perform redundant synaptic functions that become apparent in Mint 1-deficient mice in inhibitory interneurons because these neurons selectively express higher levels of Mint 1 than Mint 2."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.252774899"xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/author | "Ho A."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/author | "Hammer R.E."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/author | "Sudhof T.C."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/author | "Malenka R.C."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/author | "Morishita W."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/pages | "1409-1414"xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/title | "A role for Mints in transmitter release: Mint 1 knockout mice exhibit impaired GABAergic synaptic transmission."xsd:string |
| http://purl.uniprot.org/citations/12547917 | http://purl.uniprot.org/core/volume | "100"xsd:string |
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