Kleymenova E, Ibraghimov-Beskrovnaya O, Kugoh H, Everitt J, Xu H, Kiguchi K, Landes G, Harris P, Walker C
Department of Carcinogenesis, University of Texas, MD Anderson Cancer Center, Science Park, Smithville, TX 78957, USA.
Mol Cell. 2001 Apr;7(4):823-32. doi: 10.1016/s1097-2765(01)00226-x.
The PKD1 gene accounts for 85% of autosomal dominant polycystic kidney disease (ADPKD), the most common human genetic disorder. Rats with a germline inactivation of one allele of the Tsc2 tumor suppressor gene developed early onset severe bilateral polycystic kidney disease, with similarities to the human contiguous gene syndrome caused by germline codeletion of PKD1 and TSC2 genes. Polycystic rat renal cells retained two normal Pkd1 alleles but were null for Tsc2 and exhibited loss of lateral membrane-localized polycystin-1. In tuberin-deficient cells, intracellular trafficking of polycystin-1 was disrupted, resulting in sequestration of polycystin-1 within the Golgi and reexpression of Tsc2 restored correct polycystin-1 membrane localization. These data identify tuberin as a determinant of polycystin-1 functional localization and, potentially, ADPKD severity.
PKD1基因导致了85%的常染色体显性多囊肾病(ADPKD),这是人类最常见的遗传疾病。种系中Tsc2肿瘤抑制基因的一个等位基因失活的大鼠,会出现早发性严重双侧多囊肾病,这与因PKD1和TSC2基因种系共缺失导致的人类相邻基因综合征相似。多囊大鼠肾细胞保留了两个正常的Pkd1等位基因,但Tsc2基因缺失,并且表现出侧膜定位的多囊蛋白-1缺失。在结节蛋白缺陷细胞中,多囊蛋白-1的细胞内运输被破坏,导致多囊蛋白-1在高尔基体中滞留,而Tsc2的重新表达恢复了多囊蛋白-1正确的膜定位。这些数据确定结节蛋白是多囊蛋白-1功能定位的决定因素,并且可能是ADPKD严重程度的决定因素。