欢迎您！东篱公司
退出
-
申报数据库
-
立项数据库
-
成果数据库
-
项目获奖数据库
中文摘要：
目的在蛋白质分子水平研究心律失常相关蛋白质M3受体与间隙连接蛋白43之间的结构相互作用,并为其作为筛选药物靶点提供依据.方法通过免疫组化结合激光共聚焦显微镜,及免疫沉淀与免疫印迹技术,研究M受体与间隙连接蛋白43的结构性共定位关系.结果证实了大鼠心室肌细胞膜蛋白中M1～M5等5个亚型的存在;观察到大鼠单个心肌细胞膜上M3受体与间隙连接蛋白43的结构性共定位;发现M受体各亚型与间隙连接蛋白43均存在结构整合,且一定浓度离子型去垢剂可破坏M3受体与间隙连接蛋白43的结构整合关系,并进一步发现参与M3受体结构整合的是间隙连接蛋白43的磷酸化形式.结论大鼠心室肌M受体亚型与间隙连接蛋白43的磷酸化形式存在结构性共定位关系,且可被一定浓度离子型去垢剂破坏.
英文摘要：
Aim To optimize the method of investigating structural integration between proteins and study the integration between arrhythmia related proteins in molecular level. Methods Immunostaining the normal ventricular myocytes was used to observe the distribution of connexin 43 and muscarinic acetylcholine receptor （mAChR）. The five mAChR subtypes were precipitated using immunoprecipitation. Then, SDS-PAGE and Western blotting with the anti-connexin 43 antibody were performed to observe whether they were structurally integrated. Further, different concentrations of detergent were used to observe whether this relationship could be broken. Results The five subtypes of mAChR existed in the cardiac myocyte of the rat, and all the five mAChR subtypes combined with connexin 43. In the normal rat ventricular myocyte membrane, connexin 43 and M3 receptor are co-located. When adding certain concentration of detergent to the membrane protein, the integration between M3 receptor and connexin 43 was broken, and the phosphorylated form of connexin 43 integrated with M3 receptor. Conclusion The results indicated that the structural integration between mAChR and phosphorylation of connexin 43 existed in rat ventricular myocardium, and this integration could be broken by certain concentration of detergent.
同期刊论文项目
同项目期刊论文
The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting H
Cardioprotective Effects and Underlying Mechanisms of Oxymatrine Against Ischemic Myocardial Injurie
JAK/STAT and PI3K/AKT Pathways Form A Mutual Transactivation Loop and Afford Resistance to Oxidative
Indapamide induces apoptosis of GH3 pituitary cells independently of its inhibition of voltage-depen
Sphingolipid Metabolite Ceramide Causes Metabolic Perturbation Contributing to HERG K+ Channel Dysfu
Large-conductance Ca2+-activated K+ currents blocke and impaired by homocysteine in human and rat me
Volume-sensitive outwardly rectifying chloride channels are involved in oxidative stress-induced apo
Increasing Intracellular calcium of guinea pig ventricular myocytes induced by platelet activating f
期刊信息
位置：