5ewl
From Proteopedia
(Difference between revisions)
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| - | '''Unreleased structure''' | ||
| - | + | ==CRYSTAL STRUCTURE OF AMINO TERMINAL DOMAINS OF THE NMDA RECEPTOR SUBUNIT GLUN1 AND GLUN2B IN COMPLEX WITH MK-22== | |
| - | + | <StructureSection load='5ewl' size='340' side='right' caption='[[5ewl]], [[Resolution|resolution]] 2.98Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[5ewl]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5EWL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5EWL FirstGlance]. <br> | |
| - | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=5SL:~{N}-[(1~{S},3~{S})-3-[3-[(4-METHYLPHENYL)METHYL]-1,2,4-OXADIAZOL-5-YL]CYCLOPENTYL]-1~{H}-PYRAZOLO[3,4-D]PYRIMIDIN-4-AMINE'>5SL</scene>, <scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=MAN:ALPHA-D-MANNOSE'>MAN</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr> | |
| - | [[ | + | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5ewj|5ewj]], [[5ewm|5ewm]]</td></tr> |
| + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5ewl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5ewl OCA], [http://pdbe.org/5ewl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5ewl RCSB], [http://www.ebi.ac.uk/pdbsum/5ewl PDBsum]</span></td></tr> | ||
| + | </table> | ||
| + | == Disease == | ||
| + | [[http://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 == | ||
| + | [[http://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: Pandit, J]] | [[Category: Pandit, J]] | ||
| + | [[Category: Allosteric inhibition]] | ||
| + | [[Category: Glun2b subunit]] | ||
| + | [[Category: Nmda receptor]] | ||
| + | [[Category: Transport protein]] | ||
Revision as of 15:25, 2 March 2016
CRYSTAL STRUCTURE OF AMINO TERMINAL DOMAINS OF THE NMDA RECEPTOR SUBUNIT GLUN1 AND GLUN2B IN COMPLEX WITH MK-22
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