Wen J K, Osumi T, Hashimoto T, Ogata M
Department of Biochemistry, Shinshu University School of Medicine, Nagano, Japan.
Physiol Chem Phys Med NMR. 1988;20(3):171-6.
In order to characterize the genetic defect in Japanese-type acatalasemia, we examined catalase synthesis in the cultured fibroblasts isolated from a patient suffering from this disease. The transcript of the mutant catalase gene was also analyzed by Northern blotting. It was demonstrated that the severe reduction in catalase protein in the acatalasemic patient is due to the defective synthesis of the enzyme caused by the lack of catalase mRNA. Using Southern blotting, we did not detect large deletion, insertion or rearrangement in the mutant catalase gene as compared with the normal one. We conclude that Japanese-type acatalasemia in this study is resulted by a small mutation in the non-coding region of catalase gene which affects some step in the catalase mRNA metabolism.
为了明确日本型无过氧化氢酶血症的基因缺陷,我们检测了从一名患有该疾病的患者分离出的培养成纤维细胞中过氧化氢酶的合成情况。还通过Northern印迹法分析了突变的过氧化氢酶基因的转录本。结果表明,无过氧化氢酶血症患者体内过氧化氢酶蛋白的严重减少是由于缺乏过氧化氢酶mRNA导致该酶合成缺陷所致。通过Southern印迹法,与正常基因相比,我们未在突变的过氧化氢酶基因中检测到大片段的缺失、插入或重排。我们得出结论,本研究中的日本型无过氧化氢酶血症是由过氧化氢酶基因非编码区的一个小突变引起的,该突变影响了过氧化氢酶mRNA代谢的某个步骤。