摘要
Calnexin/Calreticulin循环与糖蛋白内质网相关性降解 (GERAD)是真核细胞内负责糖蛋白折叠质量的重要监控机制 ,监督糖蛋白在内质网中空间构象的正确折叠 ,促进未完全折叠糖蛋白再折叠 ,错误折叠糖蛋白经GERAD途径被降解。内质网应激引起内质网功能障碍时 ,Calnexin/Calreticulin循环和 (或 )GERAD发生异常 ,错误折叠的糖蛋白在内质网堆积导致细胞功能障碍和某些疾病的发生。错误折叠糖蛋白从Calnexin/Calreticulin循环释放到GERAD一系列途径的分子机理现已逐渐明了 ,了解糖蛋白Calnexin/Calreticulin循环与内质网相关性降解过程对进一步设计针对病毒性肝炎、帕金森病等疾病的治疗方案有重要的指导意义。
In eukaryotic endoplasmic reticulum (ER), Calnexin and/or Calreticulin cycle and glycoprotein ER-associated degradation both serve the same quality-control mechanism for glycoprotein proper configuration, which superintends structural folding process, and makes the unassembled subunits of glycoprotein refold. Misfolded glycoproteins have to be degraded via a mechanism known as glycoprotein ER-associated degradation if they can not be properly folded. However, malfunction in ER resulting from endoplasmic reticulum stress might lead to further disturbances in Calnexin and/or Calreticulin cycle and GERAD, thereafter, those accumulated misfolded glycoproteins in the case of ER stress lead to the dysfunction of the cells and some diseases. An better understanding of Calnexin and/or Calreticulin cycle and GERAD mechanism can help clinicians treat such diseases as viral hepatitis, Parkinson's disease etc.
出处
《医学分子生物学杂志》
CAS
CSCD
2004年第5期298-301,共4页
Journal of Medical Molecular Biology
基金
国家自然科学基金 (No 3 0 0 70 3 0 8)
