https://scholars.lib.ntu.edu.tw/handle/123456789/160276
Title: | Regulation of inflammation by DAPK | Authors: | Lai, Ming-Zong Chen, Ruey-Hwa |
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. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/278919 | DOI: | 10.1007/s10495-013-0933-4 |
Appears in Collections: | 分子醫學研究所 |
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