mtRF1a is a human mitochondrial translation release factor decoding the major termination codons UAA and UAG.

mtRF1a is a human mitochondrial translation release factor decoding the major termination codons UAA and UAG.
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DOI:
10.1016/j.molcel.2007.06.031
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发表时间:
2007-09-07
期刊:
影响因子:
16
通讯作者:
Chrzanowska-Lightowlers Z
Chrzanowska-Lightowlers Z
中科院分区:
生物学1区
文献类型:
--
作者:
Soleimanpour-Lichaei HR;Kühl I;Gaisne M;Passos JF;Wydro M;Rorbach J;Temperley R;Bonnefoy N;Tate W;Lightowlers R;Chrzanowska-Lightowlers Z

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人类线粒体含有自己的基因组,编码13种在细胞器内合成的多肽。控制和促进这种线粒体翻译的分子过程仍不清楚。许多关键因素还没有被描述,例如,翻译终止所需的因素。所有其他系统都有两类释放因子,它们要么促进肽基-tRNA的密码子特异性水解(I类),要么缺乏特异性但刺激I类因子从核糖体解离(II类)。一种人类线粒体蛋白先前已通过计算机模拟鉴定为I类释放因子的推定成员。虽然我们不能确认这个因素的功能,我们报告的一个不同的线粒体蛋白,mtRF 1a,这是能够在体外和体内终止翻译UAA/UAG密码子的鉴定。此外,HeLa细胞中的mtRF 1a耗尽导致半乳糖生长受损和活性氧产生增加。
Human mitochondria contain their own genome, encoding 13 polypeptides that are synthesized within the organelle. The molecular processes that govern and facilitate this mitochondrial translation remain unclear. Many key factors have yet to be characterized—for example, those required for translation termination. All other systems have two classes of release factors that either promote codon-specific hydrolysis of peptidyl-tRNA (class I) or lack specificity but stimulate the dissociation of class I factors from the ribosome (class II). One human mitochondrial protein has been previously identified in silico as a putative member of the class I release factors. Although we could not confirm the function of this factor, we report the identification of a different mitochondrial protein, mtRF1a, that is capable in vitro and in vivo of terminating translation at UAA/UAG codons. Further, mtRF1a depletion in HeLa cells led to compromised growth in galactose and increased production of reactive oxygen species.
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