Inauen Corinne, Rüfenacht Véronique, Pandey Amit V, Hu Liyan, Blom Henk, Nuoffer Jean-Marc, Häberle Johannes
Division of Metabolism and Children's Research Centre (CRC), University Children's Hospital Zürich, Steinwiesstr. 75, 8032, Zurich, Switzerland.
Pediatric Endocrinology, University Children's Hospital and Department of Clinical Research, University of Bern, Bern, Switzerland.
Mol Diagn Ther. 2016 Apr;20(2):125-33. doi: 10.1007/s40291-015-0182-z.
Cysteamine is used to treat cystinosis via the modification of cysteine residues substituting arginine in mutant proteins.
We investigated the effect of cysteamine on mutant argininosuccinate lyase (ASL), the second most common defect in the urea cycle.
In an established mammalian expression system, 293T cell lysates were produced after transfection with all known cysteine for arginine mutations in the ASL gene (p.Arg94Cys, p.Arg95Cys, p.Arg168Cys, p.Arg379Cys, and p.Arg385Cys), allowing testing of the effect of cysteamine over 48 h in the culture medium as well as for 1 h immediately prior to the enzyme assay.
Cysteamine at low concentrations showed no effect on 293T cell viability, ASL protein expression, or ASL activity when applied during cell culture. However, incubation of transfected cells with 0.05 mM cysteamine immediately before the enzyme assay resulted in increased ASL activity of p.Arg94Cys, p.Arg379Cys, and p.Arg385Cys by 64, 20, and 197 %, respectively, and this result was significant (p < 0.01). Cell lysates carrying p.Arg385Cys and treated with cysteamine recover enzyme activity that is similar to the untreated designed mutation p.Arg385Lys, providing circumstantial evidence for the assumed cysteamine-induced change of a cysteine to a lysine analogue.
Since 12 % of all known genotypes in ASL deficiency are affected by a cysteine for arginine mutation, we conclude that the potential of cysteamine or of related substances as remedy for this disease should be investigated further.
半胱胺通过修饰突变蛋白中取代精氨酸的半胱氨酸残基来治疗胱氨酸病。
我们研究了半胱胺对突变型精氨酸琥珀酸裂解酶(ASL)的影响,ASL是尿素循环中第二常见的缺陷。
在一个成熟的哺乳动物表达系统中,用ASL基因中所有已知的半胱氨酸取代精氨酸突变(p.Arg94Cys、p.Arg95Cys、p.Arg168Cys、p.Arg379Cys和p.Arg385Cys)转染后制备293T细胞裂解物,从而能够在培养基中检测48小时内以及酶测定前立即检测1小时内半胱胺的作用。
在细胞培养过程中应用低浓度半胱胺对293T细胞活力、ASL蛋白表达或ASL活性均无影响。然而,在酶测定前立即用0.05 mM半胱胺孵育转染细胞,导致p.Arg94Cys、p.Arg379Cys和p.Arg385Cys的ASL活性分别增加64%、20%和197%,且该结果具有统计学意义(p < 0.01)。携带p.Arg385Cys并经半胱胺处理的细胞裂解物恢复的酶活性与未处理的设计突变p.Arg385Lys相似,为假定的半胱胺诱导的半胱氨酸向赖氨酸类似物的变化提供了间接证据。
由于ASL缺乏症中所有已知基因型的12%受半胱氨酸取代精氨酸突变的影响,我们得出结论,应进一步研究半胱胺或相关物质作为该疾病治疗方法的潜力。