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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 Proteins (3) and many more products for this protein.
Showing 10 out of 74 products:
Cow (Bovine) Polyclonal KCNN4 Primary Antibody for WB - ABIN2776147
Gao, Chotoo, Balut, Sun, Bailey, Devor: Role of S3 and S4 transmembrane domain charged amino acids in channel biogenesis and gating of KCa2.3 and KCa3.1. in The Journal of biological chemistry 2008
Human Polyclonal KCNN4 Primary Antibody for WB - ABIN948055
Wong, Roberts, Randall: Sex differences in endothelial function in porcine coronary arteries: a role for H2O2 and gap junctions? in British journal of pharmacology 2014
Human Polyclonal KCNN4 Primary Antibody for IHC, IHC (p) - ABIN4328499
Rabjerg, Oliván-Viguera, Hansen, Jensen, Sevelsted-Møller, Walter, Jensen, Marcussen, Köhler: High expression of KCa3.1 in patients with clear cell renal carcinoma predicts high metastatic risk and poor survival. in PLoS ONE 2015
Human Polyclonal KCNN4 Primary Antibody for IF (p), IHC (p) - ABIN719786
Zhang, Yang, Yin, Yi, Shen, Zhao, Zhu, Liu: Inhibition of SK4 Potassium Channels Suppresses Cell Proliferation, Migration and the Epithelial-Mesenchymal Transition in Triple-Negative Breast Cancer Cells. in PLoS ONE 2016
Blockade of K(Ca)3.1 by delivery of TRAM (show TRAM1 Antibodies)-34 via balloon catheter prevented smooth muscle phenotypic modulation and limited subsequent restenosis in a swine model.
Findings suggest that SK4 channels are expressed in triple-negative breast cancer (TNBC) cells and are involved in the proliferation, apoptosis, migration and epithelial-mesenchymal transition processes of TNBC cells.
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.
KCa3.1 in human immature dendritic cells play a major role in their migration and constitute an attractive target for the cell therapy optimization
The results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies)/mTOR (show FRAP1 Antibodies) signaling pathways.
that KCa3.1 channels are key actors in the migration capacity of neutrophils, and its inhibition did not affect other relevant cellular functions
KCa3.1 and CFTR (show CFTR Antibodies) colocalize at the plasma membrane.
KCNN4 inhibition differentially regulates migration of intestinal epithelial cells in inflamed vs. non-inflamed conditions in a PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies)-mediated manner.
KCa3.1 protein expression was increased in asthmatic compared to healthy airway epithelium in situ, and KCa3.1 currents were larger in asthmatic compared to healthy HBECs cultured in vitro
Data show that calcium-dependent potassium channel (show KCNAB2 Antibodies) KCa3.1 operates as a positive feedback mechanism for intracellular Ca2 (show CA2 Antibodies)+ increase.
high KCa3.1-mRNA expression levels were indicative of low disease specific survival of ccRCC patients, short progression-free survival, and a high metastatic potential. Therefore, KCa3.1 is of prognostic value in ccRCC
Blood brain barrier endothelial cells exhibit KCa3.1 protein and activity.
The results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt (show AKT1 Antibodies)/mTOR (show FRAP1 Antibodies) signaling pathways.
These results indicate that IK1 channels do not mediate the a slow afterhyperpolarization in pyramidal neurons.
KCa3.1 is a possible marker of M/MPhi in the protumor state and a potential therapeutic target to induce glioma-associated microglia/macrophages to re-acquire a pro-inflammatory, antitumor activity.
promotes B lymphocyte (show AKAP17A Antibodies) activation, proliferation and monocyte chemotaxis
Modulation of PKA and PI3KC2beta activity to control of KCa3.1 channel expression can be an alternative important target to attenuate ascending thoracic aortic aneurysms in Fabry disease.
These findings suggest that the KCa3.1 channel can serve as a new target to attenuate and prevent development of ascending thoracic aortic aneurysm in Fabry disease.
NDPKB/SK4 signaling is required for neointima formation in injured carotid arteries.
KCa (show CSN3 Antibodies) 3.1 blockade strongly reduced the growth of xenografted NSCLC cells.
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