Evidence map›Paper›PMID 21468027›Full record

ArticleThe EMBO journal2011

Mitochondria regulate autophagy by conserved signalling pathways.

Martin Graef, Jodi Nunnari

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

105 citing papers in PubMed, 183 citations in OpenAlex.

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  12. Contrasting views on the role of AMPK in autophagy.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
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45 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Martin GraefDepartment of Molecular and Cellular Biology, Davis University of California, Davis, CA, USA.
Jodi Nunnari
University of California, Davis · US

Funding

The Mechanism of Mitochondrial Fission and Fusion.R01GM062942 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI NUNNARI, JODI M. · 2001 to 2013
$3.9M
NIGMS NIH HHS R01 GM062942NIGMS NIH HHS R01GM062942
6 · The paper itself

Abstract

Autophagy is a conserved degradative process that is crucial for cellular homeostasis and cellular quality control via the selective removal of subcellular structures such as mitochondria. We demonstrate that a regulatory link exists between mitochondrial function and autophagy in Saccharomyces cerevisiae. During amino-acid starvation, the autophagic response consists of two independent regulatory arms-autophagy gene induction and autophagic flux-and our analysis indicates that mitochondrial respiratory deficiency severely compromises both. We show that the evolutionarily conserved protein kinases Atg1, target of rapamycin kinase complex I, and protein kinase A (PKA) regulate autophagic flux, whereas autophagy gene induction depends solely on PKA. Within this regulatory network, mitochondrial respiratory deficiency suppresses autophagic flux, autophagy gene induction, and recruitment of the Atg1-Atg13 kinase complex to the pre-autophagosomal structure by stimulating PKA activity. Our findings indicate an interrelation of two common risk factors-mitochondrial dysfunction and autophagy inhibition-for ageing, cancerogenesis, and neurodegeneration.

Indexed as

AutophagyAmino AcidsAutophagy-Related ProteinsCell RespirationCyclic AMP-Dependent Protein KinasesGene Expression Regulation, FungalMitochondriaModels, BiologicalProtein KinasesProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionAmino AcidsATG1 protein, S cerevisiaeAutophagy-Related ProteinsCyclic AMP-Dependent Protein KinasesProtein KinasesProtein Serine-Threonine KinasesSaccharomyces cerevisiae Proteinstarget of rapamycin protein, S cerevisiae

Identifiers

PMID21468027
PMCPMC3117638
OpenAlexW2171810396

What OpenQuestion holds

Textmetadata
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.