ReviewFrontiers in physiology2013
Pharmacological rescue of trafficking-impaired ATP-sensitive potassium channels.
Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed.
- A loss-of-function mutation in KCNJ11 causing sulfonylurea-sensitive diabetes in early adult life.Diabetologia · 2024Article
- Patient-Derived Cellular Models for Polytarget Precision Medicine in Pantothenate Kinase-Associated Neurodegeneration.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Beneficial effects of chronic mexiletine treatment in a human model of SCN5A overlap syndrome.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- Carbamazepine promotes surface expression of mutant Kir6.2-A28V ATP-sensitive potassium channels by modulating Golgi retention and autophagy.The Journal of biological chemistry · 2022Article
- Membrane physiology and biophysics-Another milestone.Frontiers in physiology · 2022Article
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Production and purification of ATP-sensitive potassium channel particles for cryo-electron microscopy.Methods in enzymology · 2021Article
- Precision Medicine in Rare Diseases.Diseases (Basel, Switzerland) · 2020Review
- Cellular and systemic mechanisms for glucose sensing and homeostasis.Pflugers Archiv : European journal of physiology · 2020Review
- Pharmacological chaperones of ATP-sensitive potassium channels: Mechanistic insight from cryoEM structures.Molecular and cellular endocrinology · 2020Review
- Novel dominant KAmerican journal of medical genetics. Part A · 2019Article
- Article
- Precision medicine in pantothenate kinase-associated neurodegeneration.Neural regeneration research · 2019Article
- Leptin-induced Trafficking of KInternational journal of molecular sciences · 2019Review
- Genetic Discovery of ATP-Sensitive KCirculation. Arrhythmia and electrophysiology · 2019Review
- Duplex signaling by CaM and Stac3 enhances CaThe Journal of general physiology · 2018Article
- The expression of KAnnals of translational medicine · 2018Article
- A new familial form of a late-onset, persistent hyperinsulinemic hypoglycemia of infancy caused by a novel mutation in KCNJ11.Channels (Austin, Tex.) · 2017Article
- Control of Kir channel gating by cytoplasmic domain interface interactions.The Journal of general physiology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
ATP-sensitive potassium (KATP) channels link cell metabolism to membrane excitability and are involved in a wide range of physiological processes including hormone secretion, control of vascular tone, and protection of cardiac and neuronal cells against ischemic injuries. In pancreatic β-cells, KATP channels play a key role in glucose-stimulated insulin secretion, and gain or loss of channel function results in neonatal diabetes or congenital hyperinsulinism, respectively. The β-cell KATP channel is formed by co-assembly of four Kir6.2 inwardly rectifying potassium channel subunits encoded by KCNJ11 and four sulfonylurea receptor 1 subunits encoded by ABCC8. Many mutations in ABCC8 or KCNJ11 cause loss of channel function, thus, congenital hyperinsulinism by hampering channel biogenesis and hence trafficking to the cell surface. The trafficking defects caused by a subset of these mutations can be corrected by sulfonylureas, KATP channel antagonists that have long been used to treat type 2 diabetes. More recently, carbamazepine, an anticonvulsant that is thought to target primarily voltage-gated sodium channels has been shown to correct KATP channel trafficking defects. This article reviews studies to date aimed at understanding the mechanisms by which mutations impair channel biogenesis and trafficking and the mechanisms by which pharmacological ligands overcome channel trafficking defects. Insight into channel structure-function relationships and therapeutic implications from these studies are discussed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.