View source for 9kgl


==Structure of KATP channel in complex with centipede toxin SpTx1==
<StructureSection load='9kgl' size='340' side='right'caption='[[9kgl]], [[Resolution|resolution]] 2.88&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[9kgl]] is a 9 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens], [https://en.wikipedia.org/wiki/Mesocricetus_auratus Mesocricetus auratus] and [https://en.wikipedia.org/wiki/Scolopendra_polymorpha Scolopendra polymorpha]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=9KGL OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9KGL 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]] 2.88&#8491;</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=GBM:5-CHLORO-N-(2-{4-[(CYCLOHEXYLCARBAMOYL)SULFAMOYL]PHENYL}ETHYL)-2-METHOXYBENZAMIDE'>GBM</scene></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=9kgl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9kgl OCA], [https://pdbe.org/9kgl PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9kgl RCSB], [https://www.ebi.ac.uk/pdbsum/9kgl PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9kgl ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/KCJ11_HUMAN KCJ11_HUMAN] MODY;Autosomal dominant hyperinsulinism due to Kir6.2 deficiency;Intermediate DEND syndrome;Transient neonatal diabetes mellitus;Permanent neonatal diabetes mellitus;DEND syndrome;Diazoxide-resistant focal hyperinsulinism due to Kir6.2 deficiency;Autosomal recessive hyperinsulinism due to Kir6.2 deficiency. 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.  The disease is caused by mutations affecting the gene represented in this entry.  Defects in KCNJ11 may contribute to non-insulin-dependent diabetes mellitus (NIDDM), also known as diabetes mellitus type 2.  The disease is caused by mutations affecting the gene represented in this entry.
== Function ==
[https://www.uniprot.org/uniprot/KCJ11_HUMAN KCJ11_HUMAN] This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium (By similarity). Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation.<ref>PMID:17855752</ref> <ref>PMID:28842488</ref> <ref>PMID:9831708</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Mesocricetus auratus]]
[[Category: Scolopendra polymorpha]]
[[Category: Chen L]]