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The α2 glycine receptor (GlyR) subunit, abundant in embryonic neurons, is replaced by α1 in the adult nervous system. The single-channel activity of homomeric α2 channels differs from that of α1-containing GlyRs, as even at the lowest glycine concentration (20 µM), openings occurred in long (>300-ms) groups with high open probability (P(open); 0.96; cell-attached recordings, HEK-expressed channels). Shut-time intervals within groups of openings were dominated by short shuttings of 5-10 µs. The lack of concentration dependence in the groups of openings suggests that they represent single activations, separated by very long shut times at low concentrations. Several putative mechanisms were fitted by maximizing the likelihood of the entire sequence of open and shut times, with exact missed-events allowance (program hjcfit). Records obtained at several glycine concentrations were fitted simultaneously. The adequacy of the different schemes was judged by the accuracy with which they predicted not only single-channel data but also the time course and concentration dependence of macroscopic responses elicited by rapid glycine applications to outside-out patches. The data were adequately described only with schemes incorporating a reaction intermediate in the activation, and the best was a flip mechanism with two binding sites and one open state. Fits with this mechanism showed that for α2 channels, the opening rate constant is very fast, ∼130,000 s(-1), much as for α1β GlyRs (the receptor in mature synapses), but the estimated true mean open time is 20 times longer (around 3 ms). The efficacy for the flipping step and the binding affinity were lower for α2 than for α1β channels, but the overall efficacies were similar. As we previously showed for α1 homomeric receptors, in α2 glycine channels, maximum P(open) is achieved when fewer than all five of the putative binding sites in the pentamer are occupied by glycine.
Pubmed ID: 21282399 RIS Download
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These programs have been written over the last 20 years for analysis of our own results. They all do some things that are still not available in any commercial program. The programs are written in protected-mode 32-bit Fortran 90, with some assembler subroutines for fast graphics, and the Gino graphics library. Thus they are essentially DOS programs, though they are usually run from Windows, either via a desktop icon (the .ico files) or in the DOS box. The manuals (now in pdf format), have now all been collected into a single document, DCMANUALS.PDF, which should be downloaded, and the bits that you need can then be printed. Note that some sections are common to many or all programs, e.g. the notes on the graph and histogram drawing subroutines, and it is important to read this before using any of the programs (though there is a lot of online help (hit F1) for the graphics, and also in SCAN. Sponsor. Our work was supported by the Wellcome Trust (project grant 074491) and the Medical Research Council (programme grant G0400869).
View all literature mentionsTHIS RESOURCE IS NO LONGER IN SERVICE. Documented on March 17, 2022. A large-scale database of genetics and genomics data associated to a web-interface and a set of methods and algorithms that can be used for mining the data in it. The database contains two categories of single nucleotide polymorphism (SNP) annotations: # Physical-based annotation where SNPs are categorized according to their position relative to genes (intronic, inter-genic, etc.) and according to linkage disequilibrium (LD) patterns (an inter-genic SNP can be annotated to a gene if it is in LD with variation in the gene). # Functional annotation where SNPs are classified according to their effects on expression levels, i.e. whether they are expression quantitative trait loci (eQTLs) for that gene. SCAN can be utilized in several ways including: (i) queries of the SNP and gene databases; (ii) analysis using the attached tools and algorithms; (iii) downloading files with SNP annotation for various GWA platforms. . eQTL files and reported GWAS from NHGRI may be downloaded.
View all literature mentionsCell line HEK293 is a Transformed cell line with a species of origin Homo sapiens (Human)
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