Evidence map›Paper›PMID 28560849›Full record

ArticleAging cell2017

Transcription factors CEP-1/p53 and CEH-23 collaborate with AAK-2/AMPK to modulate longevity in Caenorhabditis elegans.

Hsin-Wen Chang, Steve Pisano, Amaresh Chaturbedi, Jennifer Chen, Sarah Gordon, Aiswarya Baruah, Siu Sylvia Lee

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  4. Inhibition of VDAC1 Rescues AMediators of inflammation · 2023
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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

7 authors at 1 institution in 1 country.

Hsin-Wen ChangDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Steve PisanoDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Amaresh ChaturbediDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Jennifer ChenDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Sarah GordonDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Aiswarya BaruahDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Siu Sylvia LeeDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA.
Cornell University · US

Funding

Systematic Analysis of C elegans Longevity DeterminantsR01AG024425 · NIA · CORNELL UNIVERSITY ITHACA · PI Siu Sylvia Lee · 2004 to 2026
$8.5M
NIA NIH HHS R01 AG024425
6 · The paper itself

Abstract

A decline in mitochondrial electron transport chain (ETC) function has long been implicated in aging and various diseases. Recently, moderate mitochondrial ETC dysfunction has been found to prolong lifespan in diverse organisms, suggesting a conserved and complex role of mitochondria in longevity determination. Several nuclear transcription factors have been demonstrated to mediate the lifespan extension effect associated with partial impairment of the ETC, suggesting that compensatory transcriptional response to be crucial. In this study, we showed that the transcription factors CEP-1/p53 and CEH-23 act through a similar mechanism to modulate longevity in response to defective ETC in Caenorhabditis elegans. Genomewide gene expression profiling comparison revealed a new link between these two transcription factors and AAK-2/AMP kinase (AMPK) signaling. Further functional analyses suggested that CEP-1/p53 and CEH-23 act downstream of AAK-2/AMPK signaling and CRTC-1 transcriptional coactivator to promote stress resistance and lifespan. As AAK-2, CEP-1, and CEH-23 are all highly conserved, our findings likely provide important insights for understanding the organismal adaptive response to mitochondrial dysfunction in diverse organisms and will be relevant to aging and pathologies with a mitochondrial etiology in human.

Indexed as

AMP-Activated Protein KinasesAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsElectron Transport Chain Complex ProteinsGene Expression ProfilingGene Expression RegulationHomeodomain ProteinsLongevityMitochondriaProtein BindingProtein Serine-Threonine KinasesSignal TransductionTrans-ActivatorsTranscription, GeneticTumor Suppressor Protein p53AAK-2 protein, C elegansAMP-Activated Protein KinasesCaenorhabditis elegans ProteinsCEH-23 protein, C elegansCEP-1 protein, C elegansCRTC-1 protein, C elegansElectron Transport Chain Complex ProteinsHomeodomain ProteinsProtein Serine-Threonine KinasesTrans-ActivatorsTumor Suppressor Protein p53agingAMPKC. elegansmitochondrial ETCp53transcription

Identifiers

PMID28560849
PMCPMC5506430
OpenAlexW2617857661

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.