7uis: Difference between revisions

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<StructureSection load='7uis' size='340' side='right'caption='[[7uis]], [[Resolution|resolution]] 2.58&Aring;' scene=''>
<StructureSection load='7uis' size='340' side='right'caption='[[7uis]], [[Resolution|resolution]] 2.58&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[7uis]] is a 2 chain structure. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=7kl4 7kl4]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7UIS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7UIS FirstGlance]. <br>
<table><tr><td colspan='2'>[[7uis]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=7kl4 7kl4]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7UIS OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7UIS FirstGlance]. <br>
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[6xoe|6xoe]]</div></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.58&#8491;</td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Calcium/calmodulin-dependent_protein_kinase Calcium/calmodulin-dependent protein kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.17 2.7.11.17] </span></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=7uis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7uis OCA], [https://pdbe.org/7uis PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7uis RCSB], [https://www.ebi.ac.uk/pdbsum/7uis PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7uis ProSAT]</span></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=7uis FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7uis OCA], [https://pdbe.org/7uis PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7uis RCSB], [https://www.ebi.ac.uk/pdbsum/7uis PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7uis ProSAT]</span></td></tr>
</table>
</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 ==
== Function ==
[[https://www.uniprot.org/uniprot/KCC2A_HUMAN KCC2A_HUMAN]] CaM-kinase II (CAMK2) is a prominent kinase in the central nervous system that may function in long-term potentiation and neurotransmitter release. Member of the NMDAR signaling complex in excitatory synapses it may regulate NMDAR-dependent potentiation of the AMPAR and synaptic plasticity (By similarity). [[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).  
[https://www.uniprot.org/uniprot/KCC2A_HUMAN KCC2A_HUMAN] CaM-kinase II (CAMK2) is a prominent kinase in the central nervous system that may function in long-term potentiation and neurotransmitter release. Member of the NMDAR signaling complex in excitatory synapses it may regulate NMDAR-dependent potentiation of the AMPAR and synaptic plasticity (By similarity).
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Calcium/calmodulin-dependent protein kinase]]
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Garman, S C]]
[[Category: Garman SC]]
[[Category: Ozden, C]]
[[Category: Ozden C]]
[[Category: Stratton, M M]]
[[Category: Stratton MM]]
[[Category: Camk2a]]
[[Category: Camkii]]
[[Category: Human]]
[[Category: Kinase]]
[[Category: Transferase]]

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