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- W2517466881 abstract "Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease associated with autoantibodies to type XVII collagen (COL17). When keratinocytes are treated with BP-IgG, COL17 internalizes into cells by way of the macropinocytosis pathway. Subsequently, the internalized COL17 is degraded and decreased from the plasma membrane. Endocytosis is important in regulating external signals into cells, in mediating signal transduction and in membrane recycling. Macropinocytosis is an endocytic pathway that is involved in the nonselective fluid uptake of extracellular fluid, in antigen presentation and in entry by pathogens. We investigated the mechanism of COL17-macropinocytosis using DJM-1 cells, a cutaneous squamous cell carcinoma cell line. The inhibition of small GTPase family members Rac1 and Cdc42 was found to strongly repress COL17 internalization; additionally the Rho inhibitor also partially blocked the internalization. Western blotting using Phostag-SDS-PAGE demonstrated high levels of COL17 phosphorylation in DJM-1 cells under steady state condition. The treatment of BP-IgG induced additional phosphorylation of COL17, which was suppressed by a conventional protein kinase C (PKC) inhibitor in a dose-dependent manner. In addition, PKC inhibitor inhibited COL17 endocytosis. The stimulation with BP-IgG increased intracellular calcium level a few seconds after that stimulation. These results indicate that COL17 internalization induced by BP-IgG is mediated by a conventional PKC pathway. In summary, BP-IgG initially binds to COL17 distributed on the plasma membrane, and COL17 are internalized by means of macropinocytic pathway related with phosphorylation of intracellular domain by PKC." @default.
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- W2517466881 date "2016-09-01" @default.
- W2517466881 modified "2023-10-16" @default.
- W2517466881 title "068 Macropinocytosis of type XVII collagen induced by bullous pemphigoid IgG is regulated by protein kinase C" @default.
- W2517466881 doi "https://doi.org/10.1016/j.jid.2016.06.086" @default.
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