Aberrant termination triggers nonsense-mediated mRNA decay.
Aberrant termination triggers nonsense-mediated mRNA decay.
复制标题
异常终止会触发无义介导的 mRNA 衰变。
DOI：
10.1042/bst20060039
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发表时间：
2006
影响因子：
3.9
通讯作者：
Jacobson,A
中科院分区：
文献类型：
--
作者：
Amrani,N;Dong,S;He,F;Ganesan,R;Ghosh,S;Kervestin,S;Li,C;Mangus,DA;Spatrick,P;Jacobson,A
NMD（无义介导的mRNA衰变）是一种细胞质量控制机制，在这种机制中，原本稳定的mRNA由于过早终止密码子的存在而不稳定。我们定义了一组内源性NMD底物，证明它们在每一轮翻译中都可用于NMD，并表明过早终止和正常终止不是等效的生化事件。过早终止是异常的，其nmd刺激缺陷可以通过拴系多(A)结合蛋白（Pab1p）或拴系eRF3（真核释放因子3）（Sup35p）的存在而逆转。因此，NMD似乎是由核糖体未能在正确配置的3 ' -UTR（非翻译区）附近终止而触发的，这一事件可能促进upf /NMD因子的结合以刺激mRNA脱帽。
NMD (nonsense-mediated mRNA decay) is a cellular quality-control mechanism in which an otherwise stable mRNA is destabilized by the presence of a premature termination codon. We have defined the set of endogenous NMD substrates, demonstrated that they are available for NMD at every round of translation, and showed that premature termination and normal termination are not equivalent biochemical events. Premature termination is aberrant, and its NMD-stimulating defects can be reversed by the presence of tethered poly(A)-binding protein (Pab1p) or tethered eRF3 (eukaryotic release factor 3) (Sup35p). Thus NMD appears to be triggered by a ribosome's failure to terminate adjacent to a properly configured 3′-UTR (untranslated region), an event that may promote binding of theUPF/NMDfactors to stimulate mRNA decapping.