核因子-κB信号通路中小泛素样修饰蛋白与2型糖尿病的关系

摘要

Sumoylation is that through a series of small ubiquitin-related modifier ( SUMO) enzymes-mediated biuchemical cascades, SUMO covalently atLaches to lysine residues of the target proteins to stable them. Target molecules are mediated by the process in their positioning and functional regulation. Clussical pathway IKKβuclear factor KB ( NF-KB) in inflammatory response approach is a key signal transduciion pathway. NF-KB has been well known as a regulator participating in inflammation and immunity reaction. Recent studies have shown that not only sumoylation of NF-KB inhibited protein ( IKBa) involves in the regulation of NF-KB signaling pathway, but SUMO cnzymes can directly mediate the regulation of target genes' transcription. Here we show the newest research about SUMO modification system, SUMO circulation and recycling of its enzymes involved in NF-KB signaling pathway and its association with type 2 diabetes.%小泛素样修饰蛋白化是通过一系列小泛素样修饰蛋白(small ubiquitin-related modifier,SUMO)酶介导的生化级联反应将SUMO共价结合于靶蛋白的赖氨酸残基上,提高蛋白质稳定性,介导靶分子定位和功能调节的过程.经典通路κB抑制蛋白激酶(inhibitory protein κB kinase β,IKKβ)/核因子κB(nuclear factors κB,NF-κB)途径是炎性反应的关键信号转导通路.而NF-κB是公认的参与炎症和免疫反应的调节因子.研究发现,不仅NF-κB抑制蛋白(inhibitory protein,IκBa)的SUMO化修饰参与NF-kB信号通路的调节,而且SUMO酶可以直接介导NF-kB对靶基因的转录调控,某些蛋白也可能与SUMO化蛋白有相互作用.文中对SUMO修饰系统、SUMO循环及参与SUMO化循环的酶对NF-kB信号通路的转录调控及其与2型糖尿病相关性研究进行综述.