Evidence map›Paper›PMID 19575768›Full record

ArticleAging cell2009

Condition-adapted stress and longevity gene regulation by Caenorhabditis elegans SKN-1/Nrf.

Riva P Oliveira, Jess Porter Abate, Kieran Dilks, Jessica Landis, Jasmine Ashraf, Coleen T Murphy, T Keith Blackwell

Open access · greenAbstract read
In one paragraph

Article in Aging cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

229 citing papers in PubMed, 361 citations in OpenAlex.

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  20. The Ancestral KEAP1-NRF Pathway in AmphioxusInternational journal of molecular sciences · 2025
    Article

169 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Riva P OliveiraSection on Developmental and Stem Cell Biology, Joslin Diabetes Center, Department of Pathology, Harvard Medical School, Harvard Stem Cell Institute, One Joslin Place, Boston, MA 02215, USA.
Jess Porter Abate
Kieran Dilks
Jessica Landis
Jasmine Ashraf
Coleen T Murphy
T Keith Blackwell
Princeton University · USJoslin Diabetes Center · USUniversidade Federal de Ouro Preto · BR

Funding

TRAINING IN DIABETES AND METABOLISMT32DK007260 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 1986 to 2026
$13.6M
SKN-1 Regulation and Oxidative Stress Resistance in C. elegansR01GM062891 · NIGMS · JOSLIN DIABETES CENTER · PI BLACKWELL, T KEITH · 2001 to 2016
$5.6M
SKN-1 functions in C elegans oxidative stress responsesF32GM070088 · NIGMS · JOSLIN DIABETES CENTER · PI GARVIN, RIVA O · 2005 to 2006
$113k
NIDDK NIH HHS DK07260NIDDK NIH HHS T32 DK007260NIGMS NIH HHS F32 GM070088NIGMS NIH HHS GM62891NIGMS NIH HHS GM70088NIGMS NIH HHS R01 GM062891
6 · The paper itself

Abstract

Studies in model organisms have identified regulatory processes that profoundly influence aging, many of which modulate resistance against environmental or metabolic stresses. In Caenorhabditis elegans, the transcription regulator SKN-1 is important for oxidative stress resistance and acts in multiple longevity pathways. SKN-1 is the ortholog of mammalian Nrf proteins, which induce Phase 2 detoxification genes in response to stress. Phase 2 enzymes defend against oxygen radicals and conjugate electrophiles that are produced by Phase 1 detoxification enzymes, which metabolize lipophilic compounds. Here, we have used expression profiling to identify genes and processes that are regulated by SKN-1 under normal and stress-response conditions. Under nonstressed conditions SKN-1 upregulates numerous genes involved in detoxification, cellular repair, and other functions, and downregulates a set of genes that reduce stress resistance and lifespan. Many of these genes appear to be direct SKN-1 targets, based upon presence of predicted SKN-binding sites in their promoters. The metalloid sodium arsenite induces skn-1-dependent activation of certain detoxification gene groups, including some that were not SKN-1-upregulated under normal conditions. An organic peroxide also triggers induction of a discrete Phase 2 gene set, but additionally stimulates a broad SKN-1-independent response. We conclude that under normal conditions SKN-1 has a wide range of functions in detoxification and other processes, including modulating mechanisms that reduce lifespan. In response to stress, SKN-1 and other regulators tailor transcription programs to meet the challenge at hand. Our findings reveal striking complexity in SKN-1 functions and the regulation of systemic detoxification defenses.

Indexed as

Gene Expression RegulationAnimalsArsenitesCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsDNA, HelminthDown-RegulationLongevityNF-E2-Related Factor 1Oligonucleotide Array Sequence AnalysisReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionRNA InterferenceRNA, Messengertert-ButylhydroperoxidearseniteArsenitesCaenorhabditis elegans ProteinsDNA-Binding ProteinsDNA, HelminthNF-E2-Related Factor 1Reactive Oxygen SpeciesRNA, Messengerskn-1 protein, C eleganstert-ButylhydroperoxideTranscription Factors

Identifiers

PMID19575768
PMCPMC2776707
OpenAlexW2083089496

What OpenQuestion holds

Textmetadata
LicenceTDM
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.