Bottomley S P, Hopkins P C, Whisstock J C
Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, 3168, Australia.
Biochem Biophys Res Commun. 1998 Oct 9;251(1):1-5. doi: 10.1006/bbrc.1998.9254.
A number of disease states are attributable to alpha1-antitrypsin polymerisation within the endoplasmic reticulum of hepatocytes and subsequent plasma deficiency. Two distinct mechanisms describing the process of alpha1-antitrypsin polymerisation have been proposed, the loop A-sheet and C-sheet mechanisms. We report fluorescence studies using alpha1-antitrypsin covalently modified with pyrene maleimide. These results in conjunction with detailed molecular modelling studies, show that alpha1-antitrypsin is capable of undergoing both loop A-sheet and loop C-sheet mechanisms of polymerisation, depending upon the in vitro buffer conditions.
许多疾病状态可归因于α1抗胰蛋白酶在肝细胞内质网内聚合以及随后的血浆缺乏。已经提出了两种描述α1抗胰蛋白酶聚合过程的不同机制，即A环片层和C环片层机制。我们报告了使用芘马来酰亚胺共价修饰的α1抗胰蛋白酶进行的荧光研究。这些结果与详细的分子建模研究相结合，表明α1抗胰蛋白酶能够根据体外缓冲条件经历A环片层和C环片层聚合机制。
