https://transhumanist.ru/index.php?action=history&feed=atom&title=KCNC4 2026-04-12T16:18:21Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=KCNC4&diff=4729&oldid=prev 2021-04-29T19:32:12Z

<p>Новая страница: «Potassium voltage-gated channel subfamily C member 4 (KSHIIIC) (Voltage-gated potassium channel subunit Kv3.4) [C1orf30] ==Publications== {{medline-entry |title...»</p> <p><b>Новая страница</b></p><div>Potassium voltage-gated channel subfamily C member 4 (KSHIIIC) (Voltage-gated potassium channel subunit Kv3.4) [C1orf30]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Targeted deletion of [i]Kcne3[/i] impairs skeletal muscle function in mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28356343<br /> |abstract=[[KCNE3]] (MiRP2) forms heteromeric voltage-gated K channels with the skeletal muscle-expressed [[KCNC4]] (K 3.4) α subunit. [i][[KCNE3]][/i] was the first reported skeletal muscle K channel disease gene, but the requirement for [i][[KCNE3]][/i] in skeletal muscle has been questioned. Here, we confirmed [[KCNE3]] transcript and protein expression in mouse skeletal muscle using [i]Kcne3[/i] tissue as a negative control. Whole-transcript microarray analysis (770,317 probes, interrogating 28,853 transcripts) findings were consistent with [i]Kcne3[/i] deletion increasing gastrocnemius oxidative metabolic gene expression and the proportion of type IIa fast-twitch oxidative muscle fibers, which was verified using immunofluorescence. The down-regulated transcript set overlapped with muscle unloading gene expression profiles (≥1.5-fold change; [i]P[/i] &lt; 0.05). Gastrocnemius K channel α subunit remodeling arising from [i]Kcne3[/i] deletion was highly specific, involving just 3 of 69 α subunit genes probed: known [[KCNE3]] partners [[KCNC4]] and [[KCNH2]] (mERG) were down-regulated, and [[KCNK4]] (TRAAK) was up-regulated ([i]P[/i] &lt; 0.05). Functionally, [i]Kcne3[/i] mice exhibited abnormal hind-limb clasping upon tail suspension (63% of [i]Kcne3[/i] mice ≥10-mo-old [i]vs.[/i] 0% age-matched [i]Kcne3[/i] littermates). Whereas 5 of 5 [i]Kcne3[/i] mice exhibited the typical biphasic decline in contractile force with repetitive stimuli of hind-limb muscle, both [i]in vivo[/i] and [i]in vitro,[/i] this was absent in 6 of 6 [i]Kcne3[/i] mice tested. Finally, myoblasts isolated from [i]Kcne3[/i] mice exhibit faster-inactivating and smaller sustained outward currents than those from [i]Kcne3[/i] mice. Thus, [i]Kcne3[/i] deletion impairs skeletal muscle function in mice.-King, E. C., Patel, V., Anand, M., Zhao, X., Crump, S. M., Hu, Z., Weisleder, N., Abbott, G. W. Targeted deletion of [i]Kcne3[/i] impairs skeletal muscle function in mice.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Down-Regulation<br /> * Female<br /> * Gene Expression Regulation<br /> * Mice<br /> * Mice, Knockout<br /> * Muscle Contraction<br /> * Muscle, Skeletal<br /> * Myoblasts<br /> * Potassium Channels, Voltage-Gated<br /> * Protein Array Analysis<br /> * Transcriptome<br /> * Up-Regulation<br /> |keywords=* Kv3.4<br /> * MiRP2<br /> * myotonia<br /> * periodic paralysis<br /> * potassium channel<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472403<br /> }}</div>

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