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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. Zusätzlich bieten wir Ihnen KCNN4 Proteine (3) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 79 products:
Human Polyclonal KCNN4 Primary Antibody für 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 für 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
Human Polyclonal KCNN4 Primary Antibody für 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
Blockade of K(Ca)3.1 by delivery of TRAM (zeige TRAM1 Antikörper)-34 via balloon catheter prevented smooth muscle phenotypic modulation and limited subsequent restenosis in a swine model.
Tumor suppressor miR (zeige MLXIP Antikörper)-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 (zeige S100A14 Antikörper) which was related to recurrence in optimally debulked serous ovarian carcinoma patients
Human arrhythmogenic calmodulin mutations impede the activation of SK2 (zeige KCNN2 Antikörper) 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 (zeige TRPC1 Antikörper) 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 (zeige ODZ1 Antikörper) 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 (zeige CA2 Antikörper)+)-activated K(+) channels in adult pacemaker function.
Implicating both KCa1.1 (zeige KCNMA1 Antikörper) 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 (zeige TLR4 Antikörper) or a combination of LPS (zeige TLR4 Antikörper) and IFN-gamma (zeige IFNG Antikörper) microglia exhibited high KV 1.3 current densities ( approximately 50 pA/pF at 40 mV) and virtually no KCa (zeige CSN3 Antikörper) 3.1 and Kir (zeige GEM Antikörper) currents, while microglia differentiated with IL-4 (zeige IL4 Antikörper) exhibited large Kir (zeige GEM Antikörper) 2.1 currents ( approximately 10 pA/pF at -120 mV). KCa (zeige CSN3 Antikörper) 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 (zeige TRPV4 Antikörper) and Ca(2 (zeige CA2 Antikörper)+)-activated SK1 (zeige SPHK1 Antikörper)/3 and IK1 K(+) channels plays a critical role in regulating the K(+)-secretory BK channel KCNMA1 (zeige KCNMA1 Antikörper) in kidney collecting duct cells.
enhanced KCa (zeige CSN3 Antikörper) 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 (zeige KCNAB2 Antikörper) (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 (zeige BNC2 Antikörper) 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 (zeige AKT1 Antikörper)/mTOR (zeige FRAP1 Antikörper) 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