CAJ | 학술논문

程序性坏死是近年来发现的一种由死亡受体介导的 caspases 非依赖性细胞死亡模式，通常在凋亡被抑制的情况下发生，具有坏死细胞的形态学特征。受体相互作用蛋白（receptor interacting protein，RIP）1和3是程序性坏死信号通路中极为重要的调节蛋白。MLKL 作为 RIP1／RIP3的下游调控物质，已被证明在 TNF 诱导的程序性坏死下游通路中起着重要作用。本文就 MLKL 的发现、生理功能及其分子机制进行综述。
정서성배사시근년래발현적일충유사망수체개도적 caspases 비의뢰성세포사망모식，통상재조망피억제적정황하발생，구유배사세포적형태학특정。수체상호작용단백（receptor interacting protein，RIP）1화3시정서성배사신호통로중겁위중요적조절단백。MLKL 작위 RIP1／RIP3적하유조공물질，이피증명재 TNF 유도적정서성배사하유통로중기착중요작용。본문취 MLKL 적발현、생리공능급기분자궤제진행종술。
Necroptosis is a novel programmed cell death mechanism which is caspase independent.It is mediated by specific signaling via a death receptor ligation.Necroptosis usuaUy arises when the apoptotic Pathway is inhibited,and is characterized by a necrotic morphology.Recently many reports have revealed that necroptosis is precisely regulated by a cellular signaling pathway,like apoptosis.Receptor interaction protein kinase l and receptor interaction protein kinase 3 kinases are the key regulators of this alternative cell death mechanism.MLKL plays an important role in TNF-induced programmed necrosis pathway.In this paper physiological function and molecular mechanism were reviewed.