期刊
PLOS ONE
卷 11, 期 4, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0154260
关键词
-
资金
- Italian Cystic Fibrosis Research Foundation [2/2010, 1/2012]
- Fondazione Cariparo (Cassa di Risparmio di Padova e Rovigo)
- UE THALAMOSS Project (Thalassemia Modular Stratification System for Personalized Therapy of B-Thalassemia) [306201-FP7-HEALTH-2012-INNOVATION-1]
- Telethon [GGP10124]
- Associazione Veneta per la Lotta alla Talassemia (AVLT), Rovigo
- LABORATORIO SISTEMA [PONa300369 MIUR]
- Ministero della Salute, Italy [098/GR-2009-1596647]
Nonsense mutations generate in-frame stop codons in mRNA leading to a premature arrest of translation. Functional consequences of premature termination codons (PTCs) include the synthesis of truncated proteins with loss of protein function causing severe inherited or acquired diseases. A therapeutic approach has been recently developed that is based on the use of chemical agents with the ability to suppress PTCs (read-through) restoring the synthesis of a functional full-length protein. Research interest for compounds able to induce read-through requires an efficient high throughput large scale screening system. We present a rapid, sensitive and quantitative method based on a dual-fluorescence reporter expressed in the yeast Saccharomyces cerevisiae to monitor and quantitate read-through at PTCs. We have shown that our novel system works equally well in detecting read-through at all three PTCs UGA, UAG and UAA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据