-
KCa3.1 channel is likely to be a critical target on the oxidative stress.
-
Diet-induced hyperhomocysteinemia enhanced myoendothelial feedback, and increased Cx37 and IK1 expression may contribute. nNOS or iNOS did not upregulate to compensate for decreased eNOS, 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-34.
-
SK4 activity is crucial for cell cycle control.
-
Following differentiation with LPS or a combination of LPS and IFN-gamma microglia exhibited high KV 1.3 current densities ( approximately 50 pA/pF at 40 mV) and virtually no KCa 3.1 and Kir currents, while microglia differentiated with IL-4 exhibited large Kir 2.1 currents ( approximately 10 pA/pF at -120 mV). KCa 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 and Ca(2+)-activated SK1/3 and IK1 K(+) channels plays a critical role in regulating the K(+)-secretory BK channel KCNMA1 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 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 (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/mTOR 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 activation, proliferation and monocyte chemotaxis
-
that KCa3.1 channels are key actors in the migration capacity of neutrophils, and its inhibition did not affect other relevant cellular functions
-
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.
