Evidence map›Paper›PMID 21118999›Full record

ArticleMolecular biology of the cell2011

NOA1 is an essential GTPase required for mitochondrial protein synthesis.

Mateusz Kolanczyk, Markus Pech, Tomasz Zemojtel, Hiroshi Yamamoto, Ivan Mikula, Maria-Antonietta Calvaruso, Mariël van den Brand, Ricarda Richter, Bjoern Fischer, Anita Ritz and 13 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  6. Article
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  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Mitoribosome Biogenesis.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Human Mitoribosome Biogenesis and Its Emerging Links to Disease.International journal of molecular sciences · 2021
    Review
  18. Review
  19. The Diseased Mitoribosome.FEBS letters · 2021
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 7 institutions in 5 countries.

Mateusz KolanczykDevelopment & Disease Group, Max Planck Institute for Molecular Genetics, 14195 Berlin, Germany. kolanshy@molgen.mpg.de
Markus Pech
Tomasz Zemojtel
Hiroshi Yamamoto
Ivan Mikula
Maria-Antonietta Calvaruso
Mariël van den Brand
Ricarda Richter
Bjoern Fischer
Anita Ritz
Nadine Kossler
Boris Thurisch
Ralf Spoerle
Jan Smeitink
Uwe Kornak
Danny Chan
Martin Vingron
Pavel Martasek
Robert N Lightowlers
Leo Nijtmans
Markus Schuelke
Knud H Nierhaus
Stefan Mundlos
Max Planck Institute for Molecular Genetics · DEMax Planck Society · DECharité - Universitätsmedizin Berlin · DERadboud University Medical Center · NLChinese University of Hong Kong · CNNewcastle University · GBWellcome Centre for Mitochondrial Research · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F011520/1Wellcome Trust 074454
6 · The paper itself

Abstract

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 in ribosomal 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 severe developmental 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 mitochondrial ribosome assembly. Furthermore, 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 adenosine triphosphate (ATP) synthesis and apoptosis.

Indexed as

Adenosine TriphosphateAnimalsApoptosisCells, CulturedEmbryo, MammalianEmbryonic DevelopmentFetal DeathFibroblastsGTP PhosphohydrolasesHumansIn Situ HybridizationMiceMice, KnockoutMitochondriaMitochondrial ProteinsOxidative PhosphorylationAdenosine TriphosphateGTP PhosphohydrolasesMitochondrial ProteinsNOA1 protein, mouseRNA, Small InterferingStaurosporine

Identifiers

PMID21118999
PMCPMC3016967
OpenAlexW2144511731

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.