ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
Genetic dissection reveals unexpected influence of beta subunits on KCNQ1 K+ channel polarized trafficking in vivo.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 32 citations in OpenAlex.
- KCNE gene family: From basic functions to diseases.Genes & diseases · 2026Review
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity.Channels (Austin, Tex.) · 2021Article
- Fluorescence Fluctuation Spectroscopy enables quantification of potassium channel subunit dynamics and stoichiometry.Scientific reports · 2021Article
- Control of Biophysical and Pharmacological Properties of Potassium Channels by Ancillary Subunits.Handbook of experimental pharmacology · 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 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
- Targeted deletion ofFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- An Exploration of Charge Compensating Ion Channels across the Phagocytic Vacuole of Neutrophils.Frontiers in pharmacology · 2017Article
- Regulation of human cardiac potassium channels by full-length KCNE3 and KCNE4.Scientific reports · 2016Article
- Novel exon 1 protein-coding regions N-terminally extend human KCNE3 and KCNE4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Kcne2 deletion attenuates acute post-ischaemia/reperfusion myocardial infarction.Cardiovascular research · 2016Article
- Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia.Scientific reports · 2016Article
- Kcne4 Deletion Sex-Dependently Alters Vascular Reactivity.Journal of vascular research · 2016Article
- Review
- Kcne2 deletion creates a multisystem syndrome predisposing to sudden cardiac death.Circulation. Cardiovascular genetics · 2014Article
- Kcne3 deletion initiates extracardiac arrhythmogenesis in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Arrhythmogenic KCNE gene variants: current knowledge and future challenges.Frontiers in genetics · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Targeted deletion of the Kcne2 potassium channel β subunit gene ablates gastric acid secretion and predisposes to gastric neoplasia in mice. Here, we discovered that Kcne2 deletion basolaterally reroutes the Kcnq1 α subunit in vivo in parietal cells (PCs), in which the normally apical location of the Kcnq1-Kcne2 channel facilitates its essential role in gastric acid secretion. Quantitative RT-PCR and Western blotting revealed that Kcne2 deletion remodeled fundic Kcne3 (2.9±0.8-fold mRNA increase, n=10; 5.3±0.4-fold protein increase, n=7) but not Kcne1, 4, or 5, and resulted in basolateral Kcnq1-Kcne3 complex formation in Kcne2(-/-) PCs. Concomitant targeted deletion of Kcne3 (creating Kcne2(-/-)Kcne3(-/-) mice) restored PC apical Kcnq1 localization without Kcne1, 4, or 5 remodeling (assessed by quantitative RT-PCR; n=5-10), indicating Kcne3 actively, basolaterally rerouted Kcnq1 in Kcne2(-/-) PCs. Despite this, Kcne3 deletion exacerbated gastric hyperplasia in Kcne2(-/-) mice, and both hypochlorhydria and hyperplasia in Kcne2(+/-) mice, suggesting that Kcne3 up-regulation was beneficial in Kcne2-depleted PCs. The findings reveal, in vivo, Kcne-dependent α subunit polarized trafficking and the existence and consequences of potassium channel β subunit remodeling.
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Registered trials
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