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亚硒酸盐性白内障中膜主要内在蛋白(MIP26)的蛋白水解变化

Proteolytic changes in main intrinsic polypeptide (MIP26) from membranes in selenite cataract.

作者信息

David L L, Takemoto L J, Anderson R S, Shearer T R

机构信息

Department of Biochemistry, Oregon Health Sciences University, Portland 97201.

出版信息

Curr Eye Res. 1988 Apr;7(4):411-7. doi: 10.3109/02713688809031791.

Abstract

Experimental nuclear cataract produced by an overdose of sodium selenite exhibited limited proteolysis, including breakdown of main intrinsic polypeptide (MIP26) to 24 and 22 kD fragments. Micro-sequencing and site specific immunologic probes were used in the present study to determine regions of cleavage in MIP26 during selenite cataractogenesis. Data suggested that proteolysis occurred in the C-terminus of MIP26. This may have lead to exposure of normally hidden amino acid residues on the C-terminal extension of MIP26. Loss of antigenicity of the N-terminus occurred. These significant changes to the MIP26 molecule might adversely affect communication between lens fiber cells and contribute to selenite cataract.

摘要

过量亚硒酸钠所致的实验性核性白内障表现出有限的蛋白水解作用,包括主要内在多肽(MIP26)降解为24kD和22kD片段。本研究使用微量测序和位点特异性免疫探针来确定亚硒酸钠致白内障过程中MIP26的裂解区域。数据表明蛋白水解发生在MIP26的C末端。这可能导致MIP26 C末端延伸区通常隐藏的氨基酸残基暴露。N末端抗原性丧失。MIP26分子的这些显著变化可能对晶状体纤维细胞间的通讯产生不利影响,并导致亚硒酸钠性白内障。

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