View source for 10fd


==SK5G-Matured in complex with GluN1-GluN2B, full refinement==
<StructureSection load='10fd' size='340' side='right'caption='[[10fd]], [[Resolution|resolution]] 3.09&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[10fd]] 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=10FD OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=10FD 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]] 3.09&#8491;</td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=10fd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=10fd OCA], [https://pdbe.org/10fd PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=10fd RCSB], [https://www.ebi.ac.uk/pdbsum/10fd PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=10fd ProSAT]</span></td></tr>
</table>
== 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).
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</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Mus musculus]]
[[Category: Furukawa HF]]
[[Category: Kleeman SO]]