ArticleThe Journal of biological chemistry2011
Kir2.6 regulates the surface expression of Kir2.x inward rectifier potassium channels.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Uncovering the genetic architecture of ME/CFS: a precision approach reveals impact of rare monogenic variation.Journal of translational medicine · 2025Article
- Phenotypic Variability of Andersen-Tawil Syndrome Due to Allelic Mutation c.652C>T in theBiomolecules · 2024Article
- Periodic paralysis.Handbook of clinical neurology · 2024Review
- Article
- Regulation of muscle potassium: exercise performance, fatigue and health implications.European journal of applied physiology · 2021Review
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Further evidence for shared genetic susceptibility in both sporadic and Thyrotoxic periodic paralysis.Journal of the neurological sciences · 2020Article
- Modeling and simulation of excitation- contraction coupling of fast-twitch skeletal muscle fibers.Technology and health care : official journal of the European Society for Engineering and Medicine · 2020Article
- IncreasedNeurology. Genetics · 2018Article
- Responses of rat and mouse primary microglia to pro- and anti-inflammatory stimuli: molecular profiles, KJournal of neuroinflammation · 2017Article
- Whole genome and exome sequencing realignment supports the assignment of KCNJ12, KCNJ17, and KCNJ18 paralogous genes in thyrotoxic periodic paralysis locus: functional characterization of two polymorphic Kir2.6 isoforms.Molecular genetics and genomics : MGG · 2016Article
- Rare KCNJ18 variants do not explain hypokalaemic periodic paralysis in 263 unrelated patients.Journal of neurology, neurosurgery, and psychiatry · 2016Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- The clinical and genetic features in a cohort of mainland Chinese patients with thyrotoxic periodic paralysis.BMC neurology · 2015Article
- Inward rectifier potassium currents in mammalian skeletal muscle fibres.The Journal of physiology · 2015Article
- Huntington disease skeletal muscle is hyperexcitable owing to chloride and potassium channel dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Thyrotoxic periodic paralysis: clinical and molecular aspects.Endocrine · 2013Review
- Cloning and functional characterization of inward-rectifying potassium (Kir) channels from Malpighian tubules of the mosquito Aedes aegypti.Insect biochemistry and molecular biology · 2013Article
- Genome-wide association study identifies a susceptibility locus for thyrotoxic periodic paralysis at 17q24.3.Nature genetics · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Precise trafficking, localization, and activity of inward rectifier potassium Kir2 channels are important for shaping the electrical response of skeletal muscle. However, how coordinated trafficking occurs to target sites remains unclear. Kir2 channels are tetrameric assemblies of Kir2.x subunits. By immunocytochemistry we show that endogenous Kir2.1 and Kir2.2 are localized at the plasma membrane and T-tubules in rodent skeletal muscle. Recently, a new subunit, Kir2.6, present in human skeletal muscle, was identified as a gene in which mutations confer susceptibility to thyrotoxic hypokalemic periodic paralysis. Here we characterize the trafficking and interaction of wild type Kir2.6 with other Kir2.x in COS-1 cells and skeletal muscle in vivo. Immunocytochemical and electrophysiological data demonstrate that Kir2.6 is largely retained in the endoplasmic reticulum, despite high sequence identity with Kir2.2 and conserved endoplasmic reticulum and Golgi trafficking motifs shared with Kir2.1 and Kir2.2. We identify amino acids responsible for the trafficking differences of Kir2.6. Significantly, we show that Kir2.6 subunits can coassemble with Kir2.1 and Kir2.2 in vitro and in vivo. Notably, this interaction limits the surface expression of both Kir2.1 and Kir2.2. We provide evidence that Kir2.6 functions as a dominant negative, in which incorporation of Kir2.6 as a subunit in a Kir2 channel heterotetramer reduces the abundance of Kir2 channels on the plasma membrane.
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