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- W2072977237 abstract "Ca2+ store depletion activates both Ca2+ selective and non-selective currents in endothelial cells. Recently, considerable progress has been made in understanding the molecular make-up and regulation of an endothelial cell thapsigargin-activated Ca2+ selective current, I(SOC). Indeed, I(SOC) is a relatively small inward Ca2+ current that exhibits an approximate +40mV reversal potential and is strongly inwardly rectifying. This current is sensitive to organization of the actin-based cytoskeleton. Transient receptor potential (TRP) proteins 1 and 4 (TRPC1 and TRPC4, respectively) each contribute to the molecular basis of I(SOC), although it is TRPC4 that appears to be tethered to the cytoskeleton through a dynamic interaction with protein 4.1. Activation of I(SOC) requires association between protein 4.1 and the actin-based cytoskeleton (mediated through spectrin), suggesting protein 4.1 mediates the physical communication between Ca2+ store depletion and channel activation. Thus, at present findings indicate a TRPC4-protein 4.1 physical linkage regulates I(SOC) activation following Ca2+ store depletion." @default.
- W2072977237 created "2016-06-24" @default.
- W2072977237 creator A5048696645 @default.
- W2072977237 creator A5062367097 @default.
- W2072977237 creator A5088002090 @default.
- W2072977237 date "2003-05-01" @default.
- W2072977237 modified "2023-10-17" @default.
- W2072977237 title "On the endothelial cell ISOC" @default.
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- W2072977237 doi "https://doi.org/10.1016/s0143-4160(03)00046-0" @default.
- W2072977237 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12765679" @default.
- W2072977237 hasPublicationYear "2003" @default.
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