| Corticotropin Releasing Factor Mediates KCa3.1 Inhibition, Hyperexcitability, and Seizures in Acquired Epilepsy. | Corticotropin Releasing Factor Mediates K(Ca)3.1 Inhibition, Hyperexcitability, and Seizures in Acquired Epilepsy.
Tiwari MN, Mohan S, Biala Y, Shor O, Benninger F, Yaari Y., Free PMC Article | 08/6/2022 |
| The intermediate-conductance calcium-activated potassium channel KCa3.1 contributes to alkalinization-induced vascular calcification in vitro. | The intermediate-conductance calcium-activated potassium channel KCa3.1 contributes to alkalinization-induced vascular calcification in vitro.
Bai Y, Xu J, Yang S, Zhang H, He L, Zhou W, Cheng M, Zhang S., Free PMC Article | 01/15/2022 |
| KCNN4 Expression Is Elevated in Inflammatory Bowel Disease: This Might Be a Novel Marker and Therapeutic Option Targeting Potassium Channels. | KCNN4 Expression Is Elevated in Inflammatory Bowel Disease: This Might Be a Novel Marker and Therapeutic Option Targeting Potassium Channels.
Süss C, Broncy L, Pollinger K, Kunst C, Gülow K, Müller M, Wölfel G. | 10/9/2021 |
| A critical role of the KCa 3.1 channel in mechanical stretch-induced proliferation of rat bone marrow-derived mesenchymal stem cells. | A critical role of the K(Ca) 3.1 channel in mechanical stretch-induced proliferation of rat bone marrow-derived mesenchymal stem cells.
Jia X, Su H, Chen X, Huang Y, Zheng Y, Ji P, Gao C, Gong X, Huang Y, Jiang LH, Fan Y., Free PMC Article | 09/11/2021 |
| Ca(2+)-activated KCa3.1 potassium channels contribute to the slow afterhyperpolarization in L5 neocortical pyramidal neurons. | Ca(2+)-activated KCa3.1 potassium channels contribute to the slow afterhyperpolarization in L5 neocortical pyramidal neurons.
Roshchin MV, Ierusalimsky VN, Balaban PM, Nikitin ES., Free PMC Article | 03/6/2021 |
| adiposederived stem cells transduced with SK4 may be used to generate biological pacemakers in ex vivo rat hearts. | Adipose‑derived stem cells overexpressing SK4 calcium‑activated potassium channel generate biological pacemakers.
Yang M, Zhao Q, Zhao H, Yang A, Wang F, Wang X, Tang Y, Huang C., Free PMC Article | 04/18/2020 |
| The present study provided evidence that SK4 and HCN2 combined could construct an ectopic pacemaker, laying the groundwork for the development of improved biological pacing mechanisms in the future. | Overexpression of the medium‑conductance calcium‑activated potassium channel (SK4) and the HCN2 channel to generate a biological pacemaker.
Zhao H, Yang M, Wang F, Yang A, Zhao Q, Wang X, Tang Y, Wang T, Huang C. | 02/8/2020 |
| KC a3.1 channels facilitate myocardial inflammation and the differentiation of bone marrow-derived monocytes into myofibroblasts in cardiac fibrosis caused by angiotensin II infusion. | K(Ca)3.1 Channels Promote Cardiac Fibrosis Through Mediating Inflammation and Differentiation of Monocytes Into Myofibroblasts in Angiotensin II -Treated Rats.
She G, Ren YJ, Wang Y, Hou MC, Wang HF, Gou W, Lai BC, Lei T, Du XJ, Deng XL., Free PMC Article | 01/4/2020 |
| expression significantly decreased in the penile corpus cavernosum of castrated groups, and expression positively correlated with level of androgen | Effect of low androgen levels on IKca and SKca3 channels in rat penile corpus cavernosum.
Zhao H, Jiang J, Xia J, Jiang R. | 02/9/2019 |
| T-cell dependency on Kv1.3 or KCa3.1 might be irreversibly modulated by antigen exposure. | Potassium channels Kv1.3 and KCa3.1 cooperatively and compensatorily regulate antigen-specific memory T cell functions.
Chiang EY, Li T, Jeet S, Peng I, Zhang J, Lee WP, DeVoss J, Caplazi P, Chen J, Warming S, Hackos DH, Mukund S, Koth CM, Grogan JL., Free PMC Article | 11/10/2018 |
| EDHF-mediated relaxations in superior mesenteric arteries are impaired in spontaneously hypertensive rats, and utilize components of BKCa in addition to SKCa/IKCa channel activities | Differential participation of calcium-activated potassium channel in endothelium-dependent hyperpolarization-type relaxation in superior mesenteric arteries of spontaneously hypertensive rats.
Ando M, Matsumoto T, Kobayashi S, Iguchi M, Taguchi K, Kobayashi T. | 11/3/2018 |
| Data suggest that KCa3.1 is involved in inflammatory changes in brain during diabetic ketoacidosis; here, an inhibitor of KCa3.1 (but not an inhibitor of sodium-potassium-chloride symporter) is effective in reducing brain inflammation (in hippocampus, cortex, and striatum) due to diabetic ketoacidosis. | Treatment with the KCa3.1 inhibitor TRAM-34 during diabetic ketoacidosis reduces inflammatory changes in the brain.
Glaser N, Little C, Lo W, Cohen M, Tancredi D, Wulff H, O'Donnell M. | 05/5/2018 |
| Kca3.1 may play a role in the development of Pulmonary artery hypertension (PAH) by activating ERK/p38 MAP kinase signaling, which may then contribute to hypoxia-induced pulmonary vascular remodeling. TRAM-34 may protect against hypoxia-induced PAH. | Involvement of Ca(2+)-activated K(+) channel 3.1 in hypoxia-induced pulmonary arterial hypertension and therapeutic effects of TRAM-34 in rats.
Guo S, Shen Y, He G, Wang T, Xu D, Wen F., Free PMC Article | 01/27/2018 |
| The hypotensive effect of FAAH inhibitor URB597 is independent of KCa2.3/KCa3.1-endothelium dependent hyperpolarization-type relaxation. | The influence of DOCA-salt hypertension and chronic administration of the FAAH inhibitor URB597 on K(Ca)2.3/K(Ca)3.1-EDH-type relaxation in rat small mesenteric arteries.
Kloza M, Baranowska-Kuczko M, Malinowska B, Karpińska O, Harasim-Symbor E, Kasacka I, Kozłowska H. | 12/16/2017 |
| data firmly establish KCa3.1 channel expression in CA1 neurons | Assessing the role of IKCa channels in generating the sAHP of CA1 hippocampal pyramidal cells.
Turner RW, Asmara H, Engbers JD, Miclat J, Rizwan AP, Sahu G, Zamponi GW., Free PMC Article | 07/29/2017 |
| opening of the IK1 channel with ZAC inhibits maladaptive tissue repair and improves cardiac function, potentially mediated by the inhibition of ischemia-activated mTOR-p70S6 signaling pathway via the IK1 channel | Opening of the inward rectifier potassium channel alleviates maladaptive tissue repair following myocardial infarction.
Liu C, Liu E, Luo T, Zhang W, He R. | 02/18/2017 |
| KCNN4 inhibition differentially regulates migration of intestinal epithelial cells in inflamed vs. non-inflamed conditions in a PI3K/Akt-mediated manner. | K+ Channel Inhibition Differentially Regulates Migration of Intestinal Epithelial Cells in Inflamed vs. Non-Inflamed Conditions in a PI3K/Akt-Mediated Manner.
Zundler S, Caioni M, Müller M, Strauch U, Kunst C, Woelfel G., Free PMC Article | 07/16/2016 |
| Demonstrate complementary roles for KCa3.1 and TRPC4 channels with extracellular matrix and beta1-integrin in the regulation of alveolar repair processes. | Complementary roles of KCa3.1 channels and β1-integrin during alveolar epithelial repair.
Girault A, Chebli J, Privé A, Trinh NT, Maillé E, Grygorczyk R, Brochiero E., Free PMC Article | 07/16/2016 |
| Inhibition of KCa3.1 with TRAM-34 downregulates fibrosis-associated gene expression in vitro, and reduces portal perfusion pressure in vivo. | K⁺-channel inhibition reduces portal perfusion pressure in fibrotic rats and fibrosis associated characteristics of hepatic stellate cells.
Freise C, Heldwein S, Erben U, Hoyer J, Köhler R, Jöhrens K, Patsenker E, Ruehl M, Seehofer D, Stickel F, Somasundaram R. | 12/19/2015 |
| These results demonstrate the presence of intronic mineralocorticoid response elements in Kcnn4 and suggest a highly cooperative interaction between multiple intronic response elements. | Multiple mineralocorticoid response elements localized in different introns regulate intermediate conductance K+ (Kcnn4) channel expression in the rat distal colon.
O'Hara B, Alvarez de la Rosa D, Rajendran VM., Free PMC Article | 08/8/2015 |
| Genetic deletion of Kcnn4 reduces macrophage multinucleation through modulation of Ca(2+) signaling, increases bone mass, and improves clinical outcome in arthritis. | Kcnn4 is a regulator of macrophage multinucleation in bone homeostasis and inflammatory disease.
Kang H, Kerloc'h A, Rotival M, Xu X, Zhang Q, D'Souza Z, Kim M, Scholz JC, Ko JH, Srivastava PK, Genzen JR, Cui W, Aitman TJ, Game L, Melvin JE, Hanidu A, Dimock J, Zheng J, Souza D, Behera AK, Nabozny G, Cook HT, Bassett JH, Williams GR, Li J, Vignery A, Petretto E, Behmoaras J., Free PMC Article | 05/30/2015 |
| Blood brain barrier endothelial cells exhibit KCa3.1 protein and activity. | Blood-brain barrier KCa3.1 channels: evidence for a role in brain Na uptake and edema in ischemic stroke.
Chen YJ, Wallace BK, Yuen N, Jenkins DP, Wulff H, O'Donnell ME., Free PMC Article | 04/25/2015 |
| Recombinant small (SK2) calcium channel and calmodulin bind with three different stoichiometries that depend on the molar ratio of 2SKp/2CaM in solution. | Calcium-dependent stoichiometries of the KCa2.2 (SK) intracellular domain/calmodulin complex in solution.
Halling DB, Kenrick SA, Riggs AF, Aldrich RW., Free PMC Article | 10/18/2014 |
| Data suggest activation of endothelial Adrb1 (beta-1-adrenoceptors) suppresses vasodilation and this is mediated through inhibition of endothelial Kcnn4 (intermediate conductance Ca-activated K channels) depressing endothelial cell hyperpolarization. | β₁-Adrenoceptor stimulation suppresses endothelial IK(Ca)-channel hyperpolarization and associated dilatation in resistance arteries.
Yarova PL, Smirnov SV, Dora KA, Garland CJ., Free PMC Article | 10/11/2014 |
| Serum from experimental diabetic rats increases expression of KCa3.1 channels and promotes proliferation and migration of non-diabetic vascular smooth muscle cells, possibly participating in the vascular remodeling of experimental diabetes. | Role of KCa3.1 channels in proliferation and migration of vascular smooth muscle cells by diabetic rat serum.
Su XL, Zhang H, Yu W, Wang S, Zhu WJ. | 03/1/2014 |