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  

SUMO and the enzymes of NF-κB signaling pathway involved in type 2 diabetes

作　　者：郭英华[1] 陈思娇[1] 宋今丹[2] 

机构地区：[1]中国医科大学附属第一医院干部工作医疗部老年医学研究室 [2]医学分子生物学研究所卫生部细胞生物学重点实验室,沈阳110001

出　　处：《医学研究生学报》2011年第5期538-541,共4页Journal of Medical Postgraduates

基　　金：辽宁省自然科学基金项目(20062102);辽宁省科技攻关项目(2007225004-3);沈阳市科学技术计划项目(1071162-9-00);辽宁省教育厅项目(2008818)

摘　　要：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 proteinκB kinaseβ,IKKβ)/核因子κB(nuclear factorsκB,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。Sumoylation is that through a series of small ubiquitin-related modifier(SUMO) enzymes-mediated biochemical cascades,SUMO covalently attaches to lysine residues of the target proteins to stable them.Target molecules are mediated by the process in their positioning and functional regulation.Classical pathway IKKβ/nuclear factor κB(NF-κB) in inflammatory response approach is a key signal transduction pathway.NF-κB has been well known as a regulator participating in inflammation and immunity reaction.Recent studies have shown that not only sumoylation of NF-κB inhibited protein(IκBa) involves in the regulation of NF-κB signaling pathway,but SUMO enzymes 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-κB signaling pathway and its association with type 2 diabetes.

关 键 词：小泛素样修饰蛋白 核因子-ΚB 2型糖尿病 

分 类 号：R[医药卫生]