2ovc: Difference between revisions
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{{STRUCTURE_2ovc| PDB=2ovc | SCENE= }} | {{STRUCTURE_2ovc| PDB=2ovc | SCENE= }} | ||
===Crystal structure of a coiled-coil tetramerization domain from Kv7.4 channels=== | |||
{{ABSTRACT_PUBMED_17329207}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/KCNQ4_HUMAN KCNQ4_HUMAN]] Defects in KCNQ4 are the cause of deafness autosomal dominant type 2A (DFNA2A) [MIM:[http://omim.org/entry/600101 600101]]. DFNA2A is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information.<ref>PMID:10025409</ref><ref>PMID:10369879</ref><ref>PMID:10571947</ref><ref>PMID:10925378</ref><ref>PMID:21242547</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/KCNQ4_HUMAN KCNQ4_HUMAN]] Probably important in the regulation of neuronal excitability. May underlie a potassium current involved in regulating the excitability of sensory cells of the cochlea. KCNQ4 channels are blocked by linopirdin, XE991 and bepridil, whereas clofilium is without significant effect. Muscarinic agonist oxotremorine-M strongly suppress KCNQ4 current in CHO cells in which cloned KCNQ4 channels were coexpressed with M1 muscarinic receptors.<ref>PMID:11245603</ref> | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:017329207</ref><references group="xtra"/> | <ref group="xtra">PMID:017329207</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Clark, K A.]] | [[Category: Clark, K A.]] | ||
