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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 (77) 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.
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 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.
This work demonstrates the critical role of SK4 Ca(2 (show CA2 Proteins)+)-activated K(+) channels in adult pacemaker function.
Implicating both KCa1.1 (show KCNMA1 Proteins) and KCa3.1 channels.
Blocking KCa3.1 suppresses plaque instability in advanced stages of atherosclerosis by inhibiting macrophage polarization toward an M1 phenotype.
Blood brain barrier endothelial cells exhibit KCa3.1 protein and activity.
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.
enhanced KCa (show CSN3 Proteins) 3.1 activity may compensate for decreased nitric oxide signaling during vascular aging.
Findings highlight a novel role for intermediate-conductance calcium-activated potassium channel (show KCNAB2 Proteins) (KCa3.1) in phenotypic modulation of reactive astrocytes and in astrocyte mobilization in response to mechanical stress, providing a potential target for therapeutic intervention in brain injuries.
alpha1D Ca and SK4 channels are coupled in the atria, and deletion of alpha1D leads to decreased SK4 mRNA and BNP secretion providing evidence for a novel role of alpha1D in atrial endocrine function
KCa3.1 blockade protects against cisplatin-induced acute kidney injury through the attenuation of apoptosis by interference with intrinsic apoptotic and endoplasmic reticulum stress-related mediators.
The results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt (show AKT1 Proteins)/mTOR (show FRAP1 Proteins) signaling pathways.
These results indicate that IK1 channels do not mediate the a slow afterhyperpolarization in pyramidal neurons.
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