|Title:||Regulation of inflammation by DAPK||Authors:||Lai, Ming-Zong
|Keywords:||DAPK;Inflammation;TNF-alpha;T cell activation;NF-kappa B;Inflammasome||Issue Date:||2014||Start page/Pages:||357-363||Source:||APOPTOSIS||Abstract:||
Death-associated protein kinase (DAPK) is a tumor suppressor and negatively regulates several activation signals. Consistent with its potential anti-inflammatory activity, DAPK promotes the formation of IFN-gamma-activated inhibitor of translation (GAIT) complex that suppresses the translation of selected inflammatory genes. DAPK has been found to inhibit tumor necrosis factor-alpha (TNF-alpha)- or lipopolysaccharides (LPS)-induced NF-kappa B activation and pro-inflammatory cytokine expression. Inflammation is always associated with T cell activation, while DAPK attenuates T cell activation by a selective suppression in T cell receptor-triggered NF-kappa B activation. Recent studies, however, also reveal a contribution of DAPK to pro-inflammatory processes. DAPK is shown to mediate pro-inflammatory signaling downstream of TNF-alpha, LPS, IL-17, or IL-32. In addition, DAPK is required for the full formation of NLRP3 inflammasome, essential for the generation of IL-1 beta and IL-18. These results suggest the complicated role of DAPK in the regulation of inflammation that is likely dependent on cell types and environmental cues.
|Appears in Collections:||分子醫學研究所|
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