AMPK对Rab-GAP的调节作用研究  

Study on the regulation of Rab-GAP by AMPK

作　　者：廖健文 岳莹莹 牛文彦[1] LIAO Jian-wen;YUE Ying-ying;NIU Wen-yan(Department of Immunology, Tianjin Medical University, Tianjin 300070, China)

机构地区：[1]天津医科大学免疫学系,天津300070

出　　处：《天津医科大学学报》2018年第2期97-100,共4页Journal of Tianjin Medical University

基　　金：国家自然科学基金资助项目(81170740);高等学校博士学科点专项基金资助项目(20121202110014);天津市科委应用基础研究重点项目(15JCZDJC35500);天津市卫计委重点攻关项目(15KG102)

摘　　要：目的:检测激活型AMPK对Rab-GAP的调节作用,明确它们之间的上下游关系。方法:激活型AMPK腺病毒(AdAMPK-CA)感染C2C12小鼠骨骼肌细胞,通过细胞成像系统测定细胞中的荧光强度,明确AMPK-CA在C2C12细胞中表达。MTS试验确定没有细胞毒性的腺病毒浓度,Western blot检测AMPK底物ACC和两个Rab-GAP(TCB1D1和TCB1D4)的磷酸化。结果:AMPK-CA显著升高ACC的磷酸化,并磷酸化TBC1D1 Thr590和TBC1D4 Ser318。结论:AMPK直接磷酸化TCB1D1和TCB1D4。Objective:To examine the effect of constitutive active AMPK on Rab-GAP phosphorylaiton to elucidate the signal relationship.Methods:Mouse C2C12skeletal muscle cells were infected with constitutive active AMPK adenovirus(Ad-AMPK-CA).The expression of AMPK in C2C12cells was observed by cell fluorescence imaging system.Cytotoxicity of the adenovirus was determined by MTS.Phosphorylations of AMPK substrate ACC and two Rab-GAPs(TCB1D1and TCB1D4)were detected by Western blot.Results:AMPK-CA significantly elevated the phosphorylations of ACC and TBC1D1Thr590and TBC1D4Ser318.Conclusion:AMPK directly could regulate TBC1D1and TBC1D4.

关 键 词：单磷酸腺苷激活蛋白激酶 TBC1D1 TBC1D4 磷酸化 

分 类 号：R392.1[医药卫生—免疫学]