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- W2069361507 abstract "Phospholipase C-γ (PLC-γ) is stimulated by epidermal growth factor via activation of the epidermal growth factor receptors. The PLC inhibitor, 3-nitrocoumarin (3-NC), selectively inhibited PLC-γ in Madin-Darby canine kidney cells without affecting the activity of PLC-β. In contrast, inhibitors of PLC-β, hexadecylphosphocholine and U73122, had no effect on the activity of PLC-γ. Inhibition of PLC-γ by 3-NC was associated with an increase in tight junction permeability across Madin-Darby canine kidney cell monolayers, as evidenced by 3-NC-induced decrease in transepithelial electrical resistance and increase in mannitol flux over a concentration range that was inhibitory to PLC-γ. An analog of 3-NC, 7-hydroxy-3-NC (7-OH-3-NC), which was inactive as an inhibitor of PLC-γ, also had no effect on tight junction permeability. Treatment with 3-NC caused punctate disruption in the cortical actin filaments. The PLC-γ inhibitor, 3-NC, but not the inactive analog, 7-OH-3-NC, caused hyperphosphorylation of the tight junction proteins, occludin, ZO-1, and ZO-2. The serine/threonine kinase inhibitor, staurosporine (50–200 nm), significantly attenuated 3-NC-induced hyperphosphorylation of ZO-2. This corresponded with attenuation by staurosporine of 3-NC-induced increase in tight junction permeability, suggesting a relationship between ZO-2 phosphorylation and tight junction permeability." @default.
- W2069361507 created "2016-06-24" @default.
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- W2069361507 date "2002-09-01" @default.
- W2069361507 modified "2023-10-12" @default.
- W2069361507 title "Phospholipase C-γ Modulates Epithelial Tight Junction Permeability through Hyperphosphorylation of Tight Junction Proteins" @default.
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- W2069361507 doi "https://doi.org/10.1074/jbc.m203134200" @default.
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