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- W2138825245 abstract "Abstract T cells from patients with lupus or treated with the lupus-inducing drug hydralazine have defective ERK phosphorylation. The reason for the impaired signal transduction is unknown but important to elucidate, because decreased T cell ERK pathway signaling causes a lupus-like disease in animal models by decreasing DNA methyltransferase expression, leading to DNA hypomethylation and overexpression of methylation-sensitive genes with subsequent autoreactivity and autoimmunity. We therefore analyzed the PMA stimulated ERK pathway phosphorylation cascade in CD4+ T cells from patients with lupus and in hydralazine-treated cells. The defect in these cells localized to protein kinase C (PKC)δ. Pharmacologic inhibition of PKCδ or transfection with a dominant negative PKCδ mutant caused demethylation of the TNFSF7 (CD70) promoter and CD70 overexpression similar to lupus and hydralazine-treated T cells. These results suggest that defective T cell PKCδ activation may contribute to the development of idiopathic and hydralazine-induced lupus through effects on T cell DNA methylation." @default.
- W2138825245 created "2016-06-24" @default.
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- W2138825245 date "2007-10-15" @default.
- W2138825245 modified "2023-10-01" @default.
- W2138825245 title "Impaired T Cell Protein Kinase Cδ Activation Decreases ERK Pathway Signaling in Idiopathic and Hydralazine-Induced Lupus" @default.
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- W2138825245 doi "https://doi.org/10.4049/jimmunol.179.8.5553" @default.
- W2138825245 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17911642" @default.
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