Abstract
Magnesium-inhibited, non-selective cation current ( I MIC) is activated by depletion of intracellular Mg 2+ and ATP. I MIC transports various divalent cations including Mg 2+ and Ca 2+, and is involved in cell viability. We investigated the effect of actin dynamics on I MIC. Formation of a stable cortical actin network by calyculin A inhibited the activation of I MIC, while the actin depolymerizing reagent, cytochalasin D, reversed the inhibition. Induction of a dense cortical actin layer by transfecting the constitutively active form of RhoA also inhibited the activation of I MIC. These results suggest that the activation of I MIC may be dynamically regulated by actin cytoskeleton rearrangement.
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