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Although most signaling responses initiated by tumor necrosis factor‐α (TNF‐α) occur in a Ca2+‐independent fashion, TNF‐α receptor signaling augments Ca2+ entry induced by Gαq/11 G‐protein coupled receptors (GPCRs) in endothelial cells and increases trans‐endothelial permeability. The signaling events involved in GPCR‐induced Ca2+ influx have been characterized and involve store‐operated Ca2+ entry...
Tumor necrosis factor-α (TNF-α) induces the transcriptional activation of numerous genes involved in the inflammatory response. The recently identified protein TRUSS was investigated for its role in TNF-α-induced activation of c-Jun-NH 2 terminal kinase (JNK) and transcription factor, AP-1. Ectopic expression of TRUSS activated JNK and AP-1 in the absence and presence of TNF-α stimulation...
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