HMRF1L is a human mitochondrial translation release factor involved in the decoding of the termination codons UAA and UAG
While all essential mammalian mitochondrial factors involved in the initiation and elongation phases of translation have been cloned and well characterized, little is known about the factors involved in the termination process. In the present work, we report the functional analysis of human mitochon...
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Published in | Genes to cells : devoted to molecular & cellular mechanisms Vol. 13; no. 5; pp. 429 - 438 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Malden, USA
Malden, USA : Blackwell Publishing Inc
01.05.2008
Blackwell Publishing Inc |
Subjects | |
Online Access | Get full text |
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Summary: | While all essential mammalian mitochondrial factors involved in the initiation and elongation phases of translation have been cloned and well characterized, little is known about the factors involved in the termination process. In the present work, we report the functional analysis of human mitochondrial translation release factors (RF). Here, we show that HMRF1, which had been previously denoted as a human mitochondrial RF, was inactive in in vitro translation system, although it is a mitochondrial protein. Instead, we identified another human mitochondrial RF candidate, HMRF1L, and demonstrated that HMRF1L is indeed a mitochondrial protein that functions specifically as an RF for the decoding of mitochondrial UAA and UAG termination codons in vitro. The identification of the functional mitochondrial RF brings us much closer to a detailed understanding of the translational termination process in mammalian mitochondria as well as to the unraveling of the molecular mechanism of diseases caused by the dys-regulation of translational termination in human mitochondria. |
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Bibliography: | http://dx.doi.org/10.1111/j.1365-2443.2008.01181.x Communicated by Yoshikazu Nakamura ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1356-9597 1365-2443 |
DOI: | 10.1111/j.1365-2443.2008.01181.x |