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  NOA1 is an essential GTPase required for mitochondrial protein synthesis

Kolanczyk, M., Pech, M., Zemojte, T., Yamamoto, H., Mikula, I., Calvaruso, M.-A., et al. (2011). NOA1 is an essential GTPase required for mitochondrial protein synthesis. Molecular Biology of the Cell, 22(1), 1-11. doi:10.1091/mbc.E10-07-0643.

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Genre: Zeitschriftenartikel
Alternativer Titel : Mol Biol Cell

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Kolanczyk, Mateusz1, Autor           
Pech, Markus2, Autor           
Zemojte, Tomasz3, Autor
Yamamoto, Hiroshi4, Autor           
Mikula, Ivan, Autor
Calvaruso, Maria-Antonietta, Autor
van den Brand, Mariel, Autor
Richter, Ricarda, Autor
Fischer, Bjoern3, Autor
Ritz, Anita3, Autor
Kossler, Nadine1, Autor           
Thurisch, Boris3, Autor
Spoerle, Ralf1, Autor           
Smeitink, Jan, Autor
Kornak, Uwe1, Autor           
Chan, Danny, Autor
Vingron, Martin5, Autor           
Martasek, Pavel, Autor
Lightowlers, Robert N., Autor
Nijtmans, Leo, Autor
Schuelke, Markus, AutorNierhaus, Knud H.6, Autor           Mundlos, Stefan1, Autor            mehr..
Affiliations:
1Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433557              
2Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433547              
3Max Planck Society, ou_persistent13              
4Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433549              
5Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479639              
6Ribosomes, Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433558              

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 Zusammenfassung: NOA1 is an evolutionarily conserved GTP binding protein, which localizes predominantly to mitochondria in mammalian cells. Based on bioinformatic analysis we predicted its possible involvement in ribosomal biogenesis, although, this had not been supported by any experimental evidence. Here we determine NOA1 function through generation of knock-out mice and in-vitro assays. NOA1 deficient mice exhibit mid-gestation lethality associated with a severe developmental defect of the embryo and trophoblast. Primary embryonic fibroblasts isolated from NOA1 knock-out embryos show deficient mitochondrial protein synthesis and a global defect of oxidative phosphorylation (OXPHOS). Additionally, Noa1-/- cells are impaired in staurosporine induced apoptosis. The analysis of mitochondrial ribosomal subunits from Noa1-/- cells by sucrose gradient centrifugation and Western blotting showed anomalous sedimentation, consistent with a defect in mitochondrial ribosome assembly. Further, in vitro experiments revealed that intrinsic NOA1 GTPase activity was stimulated by bacterial ribosomal constituents. Taken together, our data show that NOA1 is required for mitochondrial protein synthesis, likely due to its yet unidentified role in mitoribosomal biogenesis. Thus, NOA1 is required for such basal mitochondrial functions as ATP synthesis and apoptosis.

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Sprache(n): eng - English
 Datum: 2011-01-01
 Publikationsstatus: Erschienen
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Titel: Molecular Biology of the Cell
  Alternativer Titel : Mol Biol Cell
Genre der Quelle: Zeitschrift
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Seiten: - Band / Heft: 22 (1) Artikelnummer: - Start- / Endseite: 1 - 11 Identifikator: ISSN: 1059-1524