Ogura H, Tani K, Kanno H, Morisaki T, Ito M, Kubonishi S, Miyazaki K, Takeuchi T, Fujii H, Miwa S
Department of Pathological Pharmacology, University of Tokyo.
Tohoku J Exp Med. 1988 May;155(1):1-9. doi: 10.1620/tjem.155.1.
Molecular analysis of four unrelated patients with Lesch-Nyhan (L-N) syndrome was performed. All four cases had typical clinical features of L-N syndrome, and the activities of hypoxanthine-guanine phosphoribosyltransferase (HPRT) were absent. No structural gene abnormalities were found by Southern blot analysis in all cases, and a decrease of HPRT mRNA was not detected by dot blot analysis in two of the four cases. However, HPRT enzyme proteins were detected by Western blot analysis in all cases. Our results showed that the production of immunologically reactive but enzymatically inactive mutant HPRT protein was pathogenic for all four patients.
对四名患有莱施-奈恩(L-N)综合征的无关患者进行了分子分析。所有四例均具有L-N综合征的典型临床特征,且次黄嘌呤-鸟嘌呤磷酸核糖基转移酶(HPRT)活性缺失。通过Southern印迹分析在所有病例中均未发现结构基因异常,并且在四例中的两例中通过斑点印迹分析未检测到HPRT mRNA的减少。然而,通过蛋白质免疫印迹分析在所有病例中均检测到了HPRT酶蛋白。我们的结果表明,产生具有免疫反应性但无酶活性的突变型HPRT蛋白对所有四名患者均具有致病性。