10ff: Difference between revisions
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Created page with "'''Unreleased structure''' The entry 10ff is ON HOLD Authors: Kleeman, S.O., Furukawa, H.F. Description: SK5A-Matured glycine/glutamate in complex with GluN1-GluN2B, full refinement Category: Unreleased Structures Category: Furukawa, H.F Category: Kleeman, S.O" |
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==SK5A-Matured glycine/glutamate in complex with GluN1-GluN2B, full refinement== | |||
<StructureSection load='10ff' size='340' side='right'caption='[[10ff]], [[Resolution|resolution]] 4.06Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[10ff]] is a 8 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=10FF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=10FF FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 4.06Å</td></tr> | |||
[[Category: | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=10ff FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=10ff OCA], [https://pdbe.org/10ff PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=10ff RCSB], [https://www.ebi.ac.uk/pdbsum/10ff PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=10ff ProSAT]</span></td></tr> | ||
[[Category: Furukawa | </table> | ||
[[Category: Kleeman | == Disease == | ||
[https://www.uniprot.org/uniprot/NMDE2_HUMAN NMDE2_HUMAN] Autosomal dominant non-syndromic intellectual disability;West syndrome. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. A chromosomal aberrations involving GRIN2B has been found in patients with mental retardation. Translocations t(9;12)(p23;p13.1) and t(10;12)(q21.1;p13.1) with a common breakpoint in 12p13.1. | |||
== Function == | |||
[https://www.uniprot.org/uniprot/NMDE2_HUMAN NMDE2_HUMAN] NMDA receptor subtype of glutamate-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. Mediated by glycine. In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage. Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death (By similarity). | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Mus musculus]] | |||
[[Category: Furukawa HF]] | |||
[[Category: Kleeman SO]] | |||
Latest revision as of 07:43, 25 March 2026
SK5A-Matured glycine/glutamate in complex with GluN1-GluN2B, full refinement
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