Barker D F, Hostikka S L, Zhou J, Chow L T, Oliphant A R, Gerken S C, Gregory M C, Skolnick M H, Atkin C L, Tryggvason K
Department of Medical Informatics, University of Utah School of Medicine, Salt Lake City 84132.
Science. 1990 Jun 8;248(4960):1224-7. doi: 10.1126/science.2349482.
X-linked Alport syndrome is a hereditary glomerulonephritis in which progressive loss of kidney function is often accompanied by progressive loss of hearing. Ultrastructural defects in glomerular basement membranes (GBM) of Alport syndrome patients implicate an altered structural protein as the cause of nephritis. The product of COL4A5, the alpha 5(IV) collagen chain, is a specific component of GBM within the kidney, and the gene maps to the same X chromosomal region as does Alport syndrome. Three structural aberrations were found in COL4A5, in intragenic deletion, a Pst I site variant, and an uncharacterized abnormality, which appear to cause nephritis and deafness, with allele-specific severity, in three Alport syndrome kindreds in Utah.
X连锁遗传性肾炎是一种遗传性肾小球肾炎,肾功能进行性丧失常伴有听力进行性丧失。Alport综合征患者肾小球基底膜(GBM)的超微结构缺陷表明,结构蛋白改变是肾炎的病因。COL4A5基因的产物α5(IV)胶原链是肾脏GBM的一种特异性成分,该基因定位于与Alport综合征相同的X染色体区域。在犹他州的三个Alport综合征家族中,在COL4A5基因中发现了三种结构异常,即基因内缺失、Pst I位点变异和一种未鉴定的异常,这些异常似乎导致了肾炎和耳聋,且具有等位基因特异性严重程度。