Suppression of eukaryotic translation termination by selected RNAs

被引：20

作者：

Carnes, J

Frolova, L

Zinnen, S

Drugeon, G

Phillippe, M

Justesen, J

Haenni, AL

Leinwand, L

Kisselev, LL

Yarus, M ^{[1
]}

机构：

[1] Univ Colorado, Dept Mol Cellular & Dev Biol, Boulder, CO 80309 USA

[2] Russian Acad Sci, Engelhardt Inst Mol Biol, Moscow 117984, Russia

[3] Ribozyme Pharmaceut Inc, Boulder, CO 80301 USA

[4] Inst Jacques Monod, F-75251 Paris 05, France

[5] CNRS UPR 41, Dept Biol Genet Dev, F-35043 Rennes, France

[6] Aarhus Univ, Dept Mol & Struct Biol, DK-8000 Aarhus C, Denmark

来源：

RNA | 2000年 / 6卷 / 10期

关键词：

aptamer; human; inhibitor; release factor; stop codon;

D O I：

10.1017/S1355838200001242

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Using selection-amplification, we have isolated RNAs with affinity for translation termination factors eRF1 and eRF1(.)eRF3 complex, Individual RNAs not only bind, but inhibit eRf1-mediated release of a model nascent chain from eukaryotic ribosomes, There is also significant but weaker inhibition of eRF1-stimulated eRF3 GTPase and eRF3 stimulation of eRF1 release activity, These latter selected RNAs therefore hinder eRF1(.)eRF3 interactions, Finally, four RNA inhibitors of release suppress a UAG stop codon in mammalian extracts dependent for termination on eRF1 from several metazoan species. These RNAs are therefore new specific inhibitors for the analysis of eukaryotic termination, and potentially a new class of omnipotent termination suppressors with possible therapeutic significance.

引用

页码：1468 / 1479

页数：12

共 55 条

[1] Mutations in RNAs of both ribosomal subunits cause defects in translation termination [J].