论文部分内容阅读
Smac(second mitochondria-derived activator of Caspase)是一种内源性促进细胞凋亡的蛋白,主要通过拮抗凋亡抑制因子(inhibitor of apoptosis proteins,IAPs)对Caspase的抑制,以及促进Caspase的催化活性从而促进凋亡,并可通过与IAPs的作用参与NF-кB的调控。IAPs在肿瘤的发生、迁移以及耐药、辐射抗性的形成中发挥重要的作用。肿瘤细胞中IAPs的高表达与其抵抗凋亡的作用相关。因此,探究Smac对IAPs的拮抗作用和对Caspase的激活机制,能够进一步阐明肿瘤细胞抗凋亡机制和其他死亡途径的逃逸机制。阐述了Smac蛋白的结构、与IAPs的相互作用以及Smac模拟物作为肿瘤放化疗增敏剂的研究。
Smac (second mitochondria-derived activator of Caspase) is an endogenous protein that promotes apoptosis mainly through inhibiting Caspase inhibition by inhibitor of apoptosis proteins (IAPs) and promoting the catalytic activity of Caspase Promote apoptosis, and participate in the regulation of NF-кB through its interaction with IAPs. IAPs play an important role in tumorigenesis, migration, drug resistance and radiation resistance. The high expression of IAPs in tumor cells is related to their anti-apoptotic effects. Therefore, exploring the antagonism of Smac to IAPs and the activation mechanism of Caspase can further clarify the anti-apoptosis mechanism of tumor cells and escape mechanisms of other death pathways. The structure of Smac protein, the interaction with IAPs and the Smac mimics were described as sensitizers of chemoradiotherapy.