ArticleThe Journal of membrane biology2009
Regulation of the Kv2.1 potassium channel by MinK and MiRP1.
Article in The Journal of membrane biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Functions of the KCNE Gene Family in Ion Channels.Biochemical genetics · 2026Review
- Functional Profiling ofCirculation. Genomic and precision medicine · 2025Article
- Combined Adaptive Immune Mechanisms Mediate Cardiac Injury After COVID-19 Vaccination.Circulation · 2025Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- Genetic risk factors for drug-induced long QT syndrome: findings from a large real-world case-control study.Pharmacogenomics · 2024Observational
- A novel loss-of-functionFrontiers in cellular neuroscience · 2024Article
- The relationship between myodural bridge, atrophy and hyperplasia of the suboccipital musculature, and cerebrospinal fluid dynamics.Scientific reports · 2023Article
- Adam, amigo, brain, and K channel.Biophysical reviews · 2023Review
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- EVAP: A two-photon imaging tool to study conformational changes in endogenous Kv2 channels in live tissues.The Journal of general physiology · 2021Article
- Severe deficiency of the voltage-gated sodium channel NaCell reports · 2021Article
- Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The unconventional biogenesis of Kv7.1-KCNE1 complexes.Science advances · 2020Article
- Spectrum of KAnnals of neurology · 2019Article
- The KCNE2 potassium channel β subunit is required for normal lung function and resilience to ischemia and reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Deletion in mice of X-linked, Brugada syndrome- and atrial fibrillation-associated Kcne5 augments ventricular KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- AKT and ERK1/2 activation via remote ischemic preconditioning prevents Kcne2-dependent sudden cardiac death.Physiological reports · 2019Article
- Remote ischemic preconditioning differentially attenuates post-ischemic cardiac arrhythmia in streptozotocin-induced diabetic versus nondiabetic rats.Cardiovascular diabetology · 2017Article
- β Subunits Control the Effects of Human Kv4.3 Potassium Channel Phosphorylation.Frontiers in physiology · 2017Article
- Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Kv2.1 is a voltage-gated potassium (Kv) channel alpha-subunit expressed in mammalian heart and brain. MinK-related peptides (MiRPs), encoded by KCNE genes, are single-transmembrane domain ancillary subunits that form complexes with Kv channel alpha-subunits to modify their function. Mutations in human MinK (KCNE1) and MiRP1 (KCNE2) are associated with inherited and acquired forms of long QT syndrome (LQTS). Here, coimmunoprecipitations from rat heart tissue suggested that both MinK and MiRP1 form native cardiac complexes with Kv2.1. In whole-cell voltage-clamp studies of subunits expressed in CHO cells, rat MinK and MiRP1 reduced Kv2.1 current density three- and twofold, respectively; slowed Kv2.1 activation (at +60 mV) two- and threefold, respectively; and slowed Kv2.1 deactivation less than twofold. Human MinK slowed Kv2.1 activation 25%, while human MiRP1 slowed Kv2.1 activation and deactivation twofold. Inherited mutations in human MinK and MiRP1, previously associated with LQTS, were also evaluated. D76N-MinK and S74L-MinK reduced Kv2.1 current density (threefold and 40%, respectively) and slowed deactivation (60% and 80%, respectively). Compared to wild-type human MiRP1-Kv2.1 complexes, channels formed with M54T- or I57T-MiRP1 showed greatly slowed activation (tenfold and fivefold, respectively). The data broaden the potential roles of MinK and MiRP1 in cardiac physiology and support the possibility that inherited mutations in either subunit could contribute to cardiac arrhythmia by multiple mechanisms.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.