Laminar flow inhibits TNF-induced ASK1 activation by preventing dissociation of ASK1 from its inhibitor 14-3-3
作者： Yingmei Liu , Guoyong Yin , James Surapisitchat , Bradford C. Berk , Wang Min
DOI: 10.1172/JCI11947
关键词:
摘要: The inflammatory cytokine TNF-α stimulates several presumed pro-atherogenic signaling events in endothelial cells (ECs), including activation of c-Jun NH2-terminal kinase (JNK) and induction E-selectin. Here, we show that apoptosis signal-regulating 1 (ASK1), a MAP kinase, is required for TNF-mediated JNK activation. TNF activates ASK1 part by dissociating from its inhibitor 14-3-3. Because the risk atherosclerosis decreased regions steady laminar flow, hypothesized flow inhibits proinflammatory cytokine-mediated JNK. Steady inhibited both Inhibition correlated with increased association A constitutively active form lacking 14-3-3-binding site (ASK1-ΔNS967A) was not flow. These data establish as target flow-mediated inhibition indicate novel role 14-3-3 an anti-inflammatory mediator ECs.
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