程序性坏死的分子机制研究进展
Research progress in molecular mechanisms of necroptosis
长期以来,人们普遍认为凋亡是生物体在生长发育以及疾病以及维持稳态过程中唯一的一种程序性死亡方式,与此同时,坏死被认为是一种不可调控的细胞死亡进程。最新的研究表明,坏死也可能是一种能够被某些特定分子通路所调控的细胞死亡方式,并将其称之为程序性坏死。程序性坏死的起始需要TNF-alpha的激活,并且RIP1和RIP3的激酶活性在其中起到很关键的所用。本文就RIP3在程序性坏死中所起的关键作用、其分子结构特性以及它与其他程序性坏死相关的信号通路分子之间的相互作用等方面的研究情况做一综述。
For a long time, apoptosis is widely believed the only way of programmed cell death in the growth and development of organism, disease, and maintain homeostasis. Meanwhile, necroptosis is considered to be a non-regulated process of cell death. Recently, many reports have revealed that necrosis may be a cell death that can be regulated by specific molecular pathway, named necroptosis. The initiation of necroptosis needs the activation of TNF-alpha, and the kinase activity of RIP1 and RIP3 play a critical role in it. In this review, the crucial role of RIP3 in necroptosis, the molecular structure characterization of it, and the interaction with other molecules of necroptosis associated signaling pathways were summarized.
丁伟、黄菊芳、钞晓培、尚蕾、李函玥
分子生物学细胞生物学
RIP3程序性坏死核因子-kappa B肿瘤坏死因子-alpha
Receptor interaction protein kinase 3necroptosisnuclear factor-kappatumor necrosis factor-alpha
丁伟,黄菊芳,钞晓培,尚蕾,李函玥.程序性坏死的分子机制研究进展[EB/OL].(2013-07-29)[2025-08-03].http://www.paper.edu.cn/releasepaper/content/201307-382.点此复制
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