2e4f: Difference between revisions
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2e4f]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E4F OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E4F FirstGlance]. <br> | <table><tr><td colspan='2'>[[2e4f]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E4F OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E4F FirstGlance]. <br> | ||
</td></tr><tr><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1n9p|1n9p]], [[1u4e|1u4e]], [[1u4f|1u4f]], [[1p7b|1p7b]]</td></tr> | </td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1n9p|1n9p]], [[1u4e|1u4e]], [[1u4f|1u4f]], [[1p7b|1p7b]]</td></tr> | ||
<tr><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">Kcnj6 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=10090 Mus musculus])</td></tr> | <tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">Kcnj6 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=10090 Mus musculus])</td></tr> | ||
<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2e4f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e4f OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2e4f RCSB], [http://www.ebi.ac.uk/pdbsum/2e4f PDBsum]</span></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=2e4f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e4f OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2e4f RCSB], [http://www.ebi.ac.uk/pdbsum/2e4f PDBsum]</span></td></tr> | ||
<table> | </table> | ||
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/IRK6_MOUSE IRK6_MOUSE]] Note=Defects in Kcnj6 are the cause of the weaver (wv) phenotype. Homozygous animals suffer from severe ataxia that is obvious by about the second postnatal week. The cerebellum of these animals is drastically reduced in size due to depletion of the major cell type of cerebellum, the granule cell neuron. Heterozygous animals are not ataxic but have an intermediate number of surviving granule cells. Male homozygotes are sterile, because of complete failure of sperm production. Both hetero- and homozygous animals undergo sporadic tonic-clonic seizures. | [[http://www.uniprot.org/uniprot/IRK6_MOUSE IRK6_MOUSE]] Note=Defects in Kcnj6 are the cause of the weaver (wv) phenotype. Homozygous animals suffer from severe ataxia that is obvious by about the second postnatal week. The cerebellum of these animals is drastically reduced in size due to depletion of the major cell type of cerebellum, the granule cell neuron. Heterozygous animals are not ataxic but have an intermediate number of surviving granule cells. Male homozygotes are sterile, because of complete failure of sperm production. Both hetero- and homozygous animals undergo sporadic tonic-clonic seizures. | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Mus musculus]] | [[Category: Mus musculus]] | ||
[[Category: Inanobe, A | [[Category: Inanobe, A]] | ||
[[Category: Kurachi, Y | [[Category: Kurachi, Y]] | ||
[[Category: Beta-barrel]] | [[Category: Beta-barrel]] | ||
[[Category: Cytoplasmic assembly]] | [[Category: Cytoplasmic assembly]] | ||
[[Category: Ion channel]] | [[Category: Ion channel]] | ||
[[Category: Transport protein]] | [[Category: Transport protein]] | ||
Revision as of 19:08, 15 January 2015
Crystal Structure of the Cytoplasmic Domain of G-Protein-Gated Inward Rectifier Potassium Channel Kir3.2Crystal Structure of the Cytoplasmic Domain of G-Protein-Gated Inward Rectifier Potassium Channel Kir3.2
Structural highlights
Disease[IRK6_MOUSE] Note=Defects in Kcnj6 are the cause of the weaver (wv) phenotype. Homozygous animals suffer from severe ataxia that is obvious by about the second postnatal week. The cerebellum of these animals is drastically reduced in size due to depletion of the major cell type of cerebellum, the granule cell neuron. Heterozygous animals are not ataxic but have an intermediate number of surviving granule cells. Male homozygotes are sterile, because of complete failure of sperm production. Both hetero- and homozygous animals undergo sporadic tonic-clonic seizures. Function[IRK6_MOUSE] This potassium channel is controlled by G proteins. It plays a role in granule cell differentiation, possibly via membrane hyperpolarization. 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. Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. See Also |
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