Sandford R, Mulroy S, Foggensteiner L
Department of Medical Genetics, Cambridge Institute of Medical Research, Addenbrooke's Hospital, UK.
Cell Mol Life Sci. 1999 Nov 15;56(7-8):567-79. doi: 10.1007/s000180050454.
Polycystin-1, polycystin-2 and polycystin-L are the predicted protein products of the PKD1, PKD2 and PKDL genes, respectively. Mutations in PKD1 and PKD2 are responsible for almost all cases of autosomal dominant polycystic kidney disease (ADPKD). This condition is one of the commonest mendelian disorders of man with a prevalence of 1:800 and is responsible for nearly 10% of cases of end-stage renal failure in adults. The cloning of PKD1 and PKD2 in recent years has provided the initial steps in defining the mechanisms underlying renal cyst formation in this condition, with the aim of defining pharmacological and genetic interventions that may ameliorate the diverse and often serious clinical manifestations of this disease. The PKD genes share regions of sequence similarity, and all predictintegral membrane proteins. Whilst the predicted protein domain structure of polycystin-1 suggests it is involved in cell-cell or cell-matrix interactions, the similarity of polycystin-2 and polycystin-L to the pore-forming domains of some cation channels suggests that they all form subunits of a large plasma membrane ion channel. In the few years since the cloning of the PKD genes, a consensus that defines the range of mutations, expression pattern, interactions and functional domains of these genes and their protein products is emerging. This review will therefore attempt to summarise these data and provide an insight in to the key areas in which polycystin research is unravelling the mechanisms involved in renal cyst formation.
多囊蛋白-1、多囊蛋白-2和多囊蛋白-L分别是PKD1、PKD2和PKDL基因的预测蛋白质产物。PKD1和PKD2的突变几乎导致了所有常染色体显性多囊肾病(ADPKD)病例。这种疾病是人类最常见的孟德尔疾病之一,患病率为1:800,占成人终末期肾衰竭病例的近10%。近年来PKD1和PKD2的克隆为确定这种疾病中肾囊肿形成的潜在机制提供了初步步骤,目的是确定可能改善这种疾病多样且往往严重的临床表现的药理学和基因干预措施。PKD基因具有序列相似区域,且均预测为整合膜蛋白。虽然多囊蛋白-1的预测蛋白质结构域表明它参与细胞间或细胞与基质的相互作用,但多囊蛋白-2和多囊蛋白-L与某些阳离子通道的孔形成结构域的相似性表明它们都构成一个大的质膜离子通道的亚基。自PKD基因克隆以来的几年里,关于这些基因及其蛋白质产物的突变范围、表达模式、相互作用和功能结构域的共识正在形成。因此,本综述将试图总结这些数据,并深入探讨多囊蛋白研究在揭示肾囊肿形成机制方面的关键领域。