ReviewBritish journal of pharmacology2009
The K+ channels K(Ca)3.1 and K(v)1.3 as novel targets for asthma therapy.
Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 75 citations in OpenAlex.
- KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Properties of Heterochannels Kv(1.1-1.2)International journal of molecular sciences · 2025Article
- KCNN4 as a genomic determinant of cytosolic delivery by the attenuated cationic lytic peptide L17E.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Sex differences in airway disease: estrogen and airway surface liquid dynamics.Biology of sex differences · 2024Review
- Regulation of T Lymphocyte Functions through Calcium Signaling Modulation by Nootkatone.International journal of molecular sciences · 2024Article
- Role of SNARE Proteins in the Insertion of KCa3.1 in the Plasma Membrane of a Polarized Epithelium.Frontiers in physiology · 2022Article
- Synthesis and biological evaluation of PET tracers designed for imaging of calcium activated potassium channel 3.1 (KRSC advances · 2021Article
- CaBritish journal of pharmacology · 2020Review
- The KCa3.1 blocker TRAM34 reverses renal damage in a mouse model of established diabetic nephropathy.PloS one · 2018Article
- Pharmacologic targeting of endothelial CaChannels (Austin, Tex.) · 2018Review
- The Role of the Cytoskeleton and Myosin-Vc in the Targeting of KCa3.1 to the Basolateral Membrane of Polarized Epithelial Cells.Frontiers in physiology · 2016Article
- Centipede venoms and their components: resources for potential therapeutic applications.Toxins · 2015Review
- Usefulness of targeting lymphocyte Kv1.3-channels in the treatment of respiratory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- Kv1.3 contains an alternative C-terminal ER exit motif and is recruited into COPII vesicles by Sec24a.BMC biochemistry · 2015Article
- Intermediate-conductance calcium-activated potassium channel KCa3.1 and chloride channel modulate chemokine ligand (CCL19/CCL21)-induced migration of dendritic cells.Translational research : the journal of laboratory and clinical medicine · 2015Article
- Article
- Human lung myofibroblast TGFβ1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3.1 K(+) channels.Fibrogenesis & tissue repair · 2015Article
- Targeted inhibition of KCa3.1 attenuates TGF-β-induced reactive astrogliosis through the Smad2/3 signaling pathway.Journal of neurochemistry · 2014Article
- Blocking KV1.3 channels inhibits Th2 lymphocyte function and treats a rat model of asthma.The Journal of biological chemistry · 2014Article
- Sequential breakdown of 3-phosphorylated phosphoinositides is essential for the completion of macropinocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Asthma affects 10% of the UK population and is an important cause of morbidity and mortality at all ages. Current treatments are either ineffective or carry unacceptable side effects for a number of patients; in consequence, development of new approaches to therapy are important. Ion channels are emerging as attractive therapeutic targets in a variety of non-excitable cells. Ion channels conducting K(+) modulate the activity of several structural and inflammatory cells which play important roles in the pathophysiology of asthma. Two channels of particular interest are the voltage-gated K(+) channel K(v)1.3 and the intermediate conductance Ca(2+)-activated K(+) channel K(Ca)3.1 (also known as IK(Ca)1 or SK4). K(v)1.3 is expressed in IFNgamma-producing T cells while K(Ca)3.1 is expressed in T cells, mast cells, macrophages, airway smooth muscle cells, fibroblasts and epithelial cells. Both channels play important roles in cell activation, migration, and proliferation through the regulation of membrane potential and calcium signalling. We hypothesize that K(Ca)3.1- and/or K(v)1.3-dependent cell processes are one of the common denominators in asthma pathophysiology. If true, these channels might serve as novel targets for the treatment of asthma. Emerging evidence lends support to this hypothesis. Further validation through the study of the role that these channels play in normal and asthmatic airway cell (patho)physiology and in vivo models will provide further justification for the assessment of small molecule blockers of K(v)1.3 and K(Ca)3.1 in the treatment of asthma.
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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.