Aminoglycosides and other factors promoting stop codon readthrough in human cells
Aminoglycosides and other factors promoting stop codon readthrough in human cells
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DOI：
10.1016/j.crvi.2006.09.001
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发表时间：
2007-01-01
影响因子：
2
通讯作者：
Jean-Jean, Olivier
中科院分区：
文献类型：
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作者：
Diop, Dialo;Chauvin, Celine;Jean-Jean, Olivier
增强的终止密码子通读是无义突变引起的疾病的潜在治疗策略。在这里，我们比较了三种因素诱导的通读水平：氨基糖苷类抗生素、抑制性 tRNA 和降低翻译终止效率的因素。我们发现，通过长期使用氨基糖苷类和抑制性 tRNA 治疗可以获得最高水平的读数，而释放因子的长期消耗仅导致读数的适度增加。我们讨论了这三种因子在治疗由过早终止密码子引起的疾病时的优点和缺点。
Enhanced stop codon readthrough is a potential treatment strategy for diseases caused by nonsense mutations. Here, we compare readthrough levels induced by three types of factors: aminoglycoside antibiotics, suppressor tRNAs, and factors decreasing translation termination efficiency. We show that the highest levels of readthrough were obtained by prolonged treatment with amino-glycosides and suppressor tRNAs, whereas prolonged depletion of release factors induced only a moderate increase in readthrough. We discuss the benefits and inconvenients of the three types of factors for their use in the therapy of diseases caused by premature stop codons.