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mtRF1a is a human mitochondrial translation release factor decoding the major termination codons UAA and UAG.
Soleimanpour-Lichaei, Hamid Reza; Kühl, Inge; Gaisne, Mauricette; Passos, Joao F; Wydro, Mateusz; Rorbach, Joanna; Temperley, Richard; Bonnefoy, Nathalie; Tate, Warren; Lightowlers, Robert; Chrzanowska-Lightowlers, Zofia.
Afiliação
  • Soleimanpour-Lichaei HR; Mitochondrial Research Group, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
Mol Cell ; 27(5): 745-57, 2007 Sep 07.
Article em En | MEDLINE | ID: mdl-17803939
ABSTRACT
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.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Fatores de Transcrição / Fatores de Terminação de Peptídeos / Códon de Terminação / Proteínas Mitocondriais Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2007 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Fatores de Transcrição / Fatores de Terminação de Peptídeos / Códon de Terminação / Proteínas Mitocondriais Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2007 Tipo de documento: Article