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The protein encoded by KCNN4 is part of a potentially heterotetrameric voltage-independent potassium channel that is activated by intracellular calcium. Additionally we are shipping KCNN4 Antibodies (87) and and many more products for this protein.
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Blockade of K(Ca)3.1 by delivery of TRAM (show TRAM1 Proteins)-34 via balloon catheter prevented smooth muscle phenotypic modulation and limited subsequent restenosis in a swine model.
this study reports cryo-electron microscopy (cryo-EM) structures of a human SK4-CaM channel complex in closed and activated states at 3.4- and 3.5-angstrom resolution, respectively.
Expression of intermediate-conductance calmodulin/calcium-activated K+ channels 3.1 (KCa3.1) mRNA and protein was detected in all three layers of the human cornea.
KCa3.1 channels are important modulators in hepatocellular homeostasis.
Tumor suppressor miR (show MLXIP Proteins)-497-5p down-regulates KCa3.1 expression and contributes to the inhibition of angiosarcoma malignancy development.
We identified a two-gene signature including KCNN4 and S100A14 (show S100A14 Proteins) which was related to recurrence in optimally debulked serous ovarian carcinoma patients
Human arrhythmogenic calmodulin mutations impede the activation of SK2 (show KCNN2 Proteins) channels in human embryonic kidney 293 cells.
This study found a very substantial functional expression of KCa3.1 channels in microglia from adult epilepsy patients.
Data show that RNAi-mediated knockdown of KCa3.1 and/or TRPC1 (show TRPC1 Proteins) leads to a significant decrease in cell proliferation due to cell cycle arrest in the G1 phase.
Higher epithelial KCNN4 expression was closely correlated with advanced TNM (show ODZ1 Proteins) stages and predicted a poor prognosis in patients with pancreatic ductal adenocarcinoma.
Here, the authors demonstrate that phosphorylation of His358 activates KCa3.1 by antagonizing copper-mediated inhibition of the channel.
Blood brain barrier endothelial cells exhibit KCa3.1 protein and activity.
Diet-induced hyperhomocysteinemia enhanced myoendothelial feedback, and increased Cx37 (show GJA4 Proteins) and IK1 expression may contribute. nNOS (show NOS1 Proteins) or iNOS (show NOS2 Proteins) did not upregulate to compensate for decreased eNOS (show NOS3 Proteins), and they had little involvement in vasomotor function.
The Intermediate-conductance calmodulin/calcium-activated K+ channels 3.1 (KCa3.1-/- knockout mice) significantly reduced corneal fibrosis and expression of pro-fibrotic marker genes, suggesting that KCa3.1 plays an important role corneal wound healing in vivo.
KCa3.1(-/-) mice exhibited significantly smaller infarct areas in a model of ischemic stroke.
KCa3.1(-/-) mice demonstrated normal behavioral responses in models of acute nociceptive, persistent inflammatory, and persistent neuropathic pain. However, their behavioral responses to noxious chemical stimuli such as formalin and capsaicin were increased. Accordingly, formalin-induced nociceptive behavior was increased in wild-type mice after administration of the KCa3.1 inhibitor TRAM (show TICAM2 Proteins)-34.
SK4 activity is crucial for cell cycle control.
Following differentiation with LPS (show TLR4 Proteins) or a combination of LPS (show TLR4 Proteins) and IFN-gamma (show IFNG Proteins) microglia exhibited high KV 1.3 current densities ( approximately 50 pA/pF at 40 mV) and virtually no KCa (show CSN3 Proteins) 3.1 and Kir (show GEM Proteins) currents, while microglia differentiated with IL-4 (show IL4 Proteins) exhibited large Kir (show GEM Proteins) 2.1 currents ( approximately 10 pA/pF at -120 mV). KCa (show CSN3 Proteins) 3.1 currents were generally low
Deletion of KCa3.1 reduced astrogliosis and rescued memory loss induced by intrahippocampal Abeta1-42 peptide injection.
Dynamic coupling between TRPV4 (show TRPV4 Proteins) and Ca(2 (show CA2 Proteins)+)-activated SK1 (show SPHK1 Proteins)/3 and IK1 K(+) channels plays a critical role in regulating the K(+)-secretory BK channel KCNMA1 (show KCNMA1 Proteins) in kidney collecting duct cells.
Blocking KCa3.1 suppresses plaque instability in advanced stages of atherosclerosis by inhibiting macrophage polarization toward an M1 phenotype.
enhanced KCa (show CSN3 Proteins) 3.1 activity may compensate for decreased nitric oxide signaling during vascular aging.
The protein encoded by this gene is part of a potentially heterotetrameric voltage-independent potassium channel that is activated by intracellular calcium. Activation is followed by membrane hyperpolarization, which promotes calcium influx. The encoded protein may be part of the predominant calcium-activated potassium channel in T-lymphocytes. This gene is similar to other KCNN family potassium channel genes, but it differs enough to possibly be considered as part of a new subfamily.
intermediate conductance calcium-activated potassium channel protein 4
, intermediate-conductance calcium-activated potassium channel
, intermediate conductance calcium-activated potassium channel protein 1
, potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4
, intermediate conductance calcium-activated potassium channel protein 4-like
, SKCa 4
, putative Gardos channel
, putative erythrocyte intermediate conductance calcium-activated potassium Gardos channel
, intermediate conductance K channel
, intermediate-conductance Ca-activated K channel
, potassium intermediate-small conductance calcium-activated channel subfamily N member 4