Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
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Experimental therapies and ongoing clinical trials to slow down progression of ADPKDNovel roles for hERG K(+) channels in cell proliferation and apoptosisNovel phenolic inhibitors of small/intermediate-conductance Ca²⁺-activated K⁺ channels, KCa3.1 and KCa2.3Using Visualized Matrix Effects to Develop and Improve LC-MS/MS Bioanalytical Methods, Taking TRAM-34 as an ExampleAdvanced glycation end products promote proliferation of cardiac fibroblasts by upregulation of KCa3.1 channelsInhibition of the K+ channel K(Ca)3.1 reduces TGF-β1-induced premature senescence, myofibroblast phenotype transition and proliferation of mesangial cells.Ca(2+)-activated K(+) channel-3.1 blocker TRAM-34 attenuates airway remodeling and eosinophilia in a murine asthma model.Down-regulation of KCa2.3 channels causes erectile dysfunction in miceTreatment strategies and clinical trial design in ADPKDEpithelial Notch signaling regulates interstitial fibrosis development in the kidneys of mice and humansIncreased constitutive αSMA and Smad2/3 expression in idiopathic pulmonary fibrosis myofibroblasts is KCa3.1-dependent.A novel pan-negative-gating modulator of KCa2/3 channels, fluoro-di-benzoate, RA-2, inhibits endothelium-derived hyperpolarization-type relaxation in coronary artery and produces bradycardia in vivo.Involvement of dominant-negative spliced variants of the intermediate conductance Ca2+-activated K+ channel, K(Ca)3.1, in immune function of lymphoid cellsThe Ca²⁺-activated K⁺ channel KCa3.1 as a potential new target for the prevention of allograft vasculopathy.The K+ channel KCa3.1 as a novel target for idiopathic pulmonary fibrosisIHG-1 promotes mitochondrial biogenesis by stabilizing PGC-1α.Fibrosis and progression of autosomal dominant polycystic kidney disease (ADPKD).Human lung myofibroblast TGFβ1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3.1 K(+) channelsSerum metabonomic analysis of protective effects of Curcuma aromatica oil on renal fibrosis rats.High expression of KCa3.1 in patients with clear cell renal carcinoma predicts high metastatic risk and poor survival.KCa3.1/IK1 Channel Regulation by cGMP-Dependent Protein Kinase (PKG) via Reactive Oxygen Species and CaMKII in Microglia: An Immune Modulating Feedback System?Modulation of K(Ca)3.1 channels by eicosanoids, omega-3 fatty acids, and molecular determinantsHydrogen Sulfide: A Therapeutic Candidate for Fibrotic Disease?The Lymphocyte Potassium Channels Kv1.3 and KCa3.1 as Targets for Immunosuppression.The Blockage of KCa3.1 Channel Inhibited Proliferation, Migration and Promoted Apoptosis of Human Hepatocellular Carcinoma CellsKCa3.1 K+ Channel Expression and Function in Human Bronchial Epithelial CellsTherapeutic potential of KCa3.1 blockers: recent advances and promising trends.KCa 3.1 channels maintain endothelium-dependent vasodilatation in isolated perfused kidneys of spontaneously hypertensive rats after chronic inhibition of NOS.Vascular KCa-channels as therapeutic targets in hypertension and restenosis disease.Identification of key metabolic changes in renal interstitial fibrosis rats using metabonomics and pharmacology.Blockade of KCa3.1 ameliorates renal fibrosis through the TGF-β1/Smad pathway in diabetic miceThe potassium channel KCa3.1 as new therapeutic target for the prevention of obliterative airway disease.Development of a QPatch automated electrophysiology assay for identifying KCa3.1 inhibitors and activators.KCa3.1 mediates activation of fibroblasts in diabetic renal interstitial fibrosis.Evidence of K+ channel function in epithelial cell migration, proliferation, and repair.Intermediate-Conductance-Ca2-Activated K Channel IKCa1 Is Upregulated and Promotes Cell Proliferation in Cervical CancerOxidative stress in obstructive nephropathy.Endothelial small-conductance and intermediate-conductance KCa channels: an update on their pharmacology and usefulness as cardiovascular targets.Role of ion transport in control of apoptotic cell death.Cell proliferation, potassium channels, polyamines and their interactions: a mini review.
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Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 13 August 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@en
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@nl
type
label
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@en
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@nl
prefLabel
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@en
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@nl
P2093
P2860
P356
P1476
Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels.
@en
P2093
Anja Müller
Anuradha Kaistha
Brajesh P Kaistha
Christoph Busch
Claudia Schmidt
Frank Strutz
Girija Raman
Heike Wulff
Hermann-Josef Gröne
P2860
P304
14518-14523
P356
10.1073/PNAS.0903458106
P407
P577
2009-08-13T00:00:00Z