Evidence map›Paper›PMID 24718614›Full record

ArticlePloS one2014

Amino acid starvation has opposite effects on mitochondrial and cytosolic protein synthesis.

Mark A Johnson, Sara Vidoni, Romina Durigon, Sarah F Pearce, Joanna Rorbach, Jiuya He, Gloria Brea-Calvo, Michal Minczuk, Aurelio Reyes, Ian J Holt and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed, 65 citations in OpenAlex.

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  20. Magnesium Is a Key Player in Neuronal Maturation and Neuropathology.International journal of molecular sciences · 2019
    Review
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

11 authors at 2 institutions in 1 country.

Mark A JohnsonMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Sara VidoniMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Romina DurigonNIMR-National Institute for Medical Research, Mill Hill, London, United Kingdom.
Sarah F PearceMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Joanna RorbachMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Jiuya HeMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Gloria Brea-CalvoMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Michal MinczukMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Aurelio ReyesMRC-Mitochondrial Biology Unit, Wellcome Trust-MRC Building, Cambridge, United Kingdom.
Ian J HoltNIMR-National Institute for Medical Research, Mill Hill, London, United Kingdom.
Antonella SpinazzolaNIMR-National Institute for Medical Research, Mill Hill, London, United Kingdom.
Wellcome Trust · GBMRC Mitochondrial Biology Unit · GB

Funding

Medical Research Council MC_PC_13029Medical Research Council MC_PC_13029/1Medical Research Council MC_U105663140Medical Research Council MC_U105697134Medical Research Council MC_U105697135Medical Research Council MC_UP_1002/1Medical Research Council MC_UP_1202/14
6 · The paper itself

Abstract

Amino acids are essential for cell growth and proliferation for they can serve as precursors of protein synthesis, be remodelled for nucleotide and fat biosynthesis, or be burnt as fuel. Mitochondria are energy producing organelles that additionally play a central role in amino acid homeostasis. One might expect mitochondrial metabolism to be geared towards the production and preservation of amino acids when cells are deprived of an exogenous supply. On the contrary, we find that human cells respond to amino acid starvation by upregulating the amino acid-consuming processes of respiration, protein synthesis, and amino acid catabolism in the mitochondria. The increased utilization of these nutrients in the organelle is not driven primarily by energy demand, as it occurs when glucose is plentiful. Instead it is proposed that the changes in the mitochondrial metabolism complement the repression of cytosolic protein synthesis to restrict cell growth and proliferation when amino acids are limiting. Therefore, stimulating mitochondrial function might offer a means of inhibiting nutrient-demanding anabolism that drives cellular proliferation.

Indexed as

Protein BiosynthesisAmino AcidsCell RespirationCytosolHEK293 CellsHumansMembrane Potential, MitochondrialMitochondriaMitochondrial ProteinsMitochondrial TurnoverRNA, MessengerAmino AcidsMitochondrial ProteinsRNA, Messenger

Identifiers

PMID24718614
PMCPMC3981720
OpenAlexW2034929921

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.