NOA1 is an essential GTPase required for mitochondrial protein synthesis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F11%3A9959" target="_blank" >RIV/00216208:11110/11:9959 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00064165:_____/11:9959

Výsledek na webu

<a href="http://dx.doi.org/10.1091/mbc.E10-07-0643" target="_blank" >http://dx.doi.org/10.1091/mbc.E10-07-0643</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

NOA1 is an essential GTPase required for mitochondrial protein synthesis

Popis výsledku v původním jazyce

Nitric oxide associated-1 (NOA1) is an evolutionarily conserved guanosine triphosphate (GTP) binding protein that localizes predominantly to mitochondria in mammalian cells. On the basis of bioinformatic analysis, we predicted its possible involvement inribosomal biogenesis, although this had not been supported by any experimental evidence. Here we determine NOA1 function through generation of knockout mice and in vitro assays. NOA1-deficient mice exhibit midgestation lethality associated with a severedevelopmental defect of the embryo and trophoblast. Primary embryonic fibroblasts isolated from NOA1 knockout 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 mitochon

Název v anglickém jazyce

NOA1 is an essential GTPase required for mitochondrial protein synthesis

Popis výsledku anglicky

Nitric oxide associated-1 (NOA1) is an evolutionarily conserved guanosine triphosphate (GTP) binding protein that localizes predominantly to mitochondria in mammalian cells. On the basis of bioinformatic analysis, we predicted its possible involvement inribosomal biogenesis, although this had not been supported by any experimental evidence. Here we determine NOA1 function through generation of knockout mice and in vitro assays. NOA1-deficient mice exhibit midgestation lethality associated with a severedevelopmental defect of the embryo and trophoblast. Primary embryonic fibroblasts isolated from NOA1 knockout 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 mitochon

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

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Projekt

<a href="/cs/project/1M0520" target="_blank" >1M0520: Centrum aplikované genomiky</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2011

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Molecular Biology of the Cell

ISSN

1059-1524

e-ISSN

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Svazek periodika

22

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

1-11

Kód UT WoS článku

000285962300001

EID výsledku v databázi Scopus

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