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Previous studies have shown that potassium channels can regulate the cytokine secretion of human activated macrophages [ 23].
Ion channels can regulate cell cycle and implication of transmembrane potassium fluxes via inward rectifier channels in the regulation of cell cycle has been proposed [ 45].
In the nervous system, BK channels can regulate neural excitability and neurotransmitter release, and the surface trafficking of BK channels can be modulated by signaling cascades and assembly with accessory proteins.
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We have shown that the L-type Ca2+ channel can regulate mitochondrial function and metabolic activity in cardiac myocytes.
Indeed, calcium influx through the SOC channel can regulate the secretion of proinflammatory molecules such as arachidonic acid and leukotriene C4 [ 25].
There can be two possible scenarios where CFTR channel function can regulate proinflammatory response: 1).
Recently, we have shown that TRPM4 channel activity can regulate cardiac contractility in the mouse heart.
In this study, we have used platelets to test whether Cl− channels in principle can regulate Ca2+-dependent PS exposure.
A large number of membrane proteins are known to be glycosyl phosphatidylinositol (GPI -anchored (Kinoshita et al, 2008), and some of them, like the channel-activatinGPI -anchoredCAP1) can regulate mechanotransduction-related channels (Vallet et al, 1997).
This controller can regulate three channels of LEDs.
It has been shown previously that M-LDH can regulate KATP channels behaviour in a recombinant heterologues expression system [1].
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