Evidence map›Paper›PMID 24691093›Full record

ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2015

Elevated ATF4 function in fibroblasts and liver of slow-aging mutant mice.

Weiquan Li, Richard A Miller

Open access · bronzeAbstract read
In one paragraph

Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

  1. Suppression rather than activation of the integrated stress response (GCN2-ATF4) pathway extends lifespan in the fly.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Multiomics ofInternational journal of molecular sciences · 2023
    Article
  8. Modulation ofAutophagy · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Recent Advances in the Systems Biology of Aging.Antioxidants & redox signaling · 2018
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Weiquan LiDepartment of Pathology and.
Richard A MillerDepartment of Pathology and Geriatrics Center, University of Michigan, Ann Arbor millerr@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Laboratory for Anti-Geric Testing, Evaluation and ResearchU01AG022303 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RICHARD A MILLER · 2003 to 2026
$25.4M
Research DevelopmentP30AG013283 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MILLER, RICHARD A · 1995 to 2014
$12.3M
The Somatotropic Axis and Health Aging: A Search for MechanismsP01AG031736 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI KIRKLAND, JAMES L. · 2009 to 2013
$8.4M
Longevity genes and calorie restriction: early post-natal effectsR01AG019899 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI BARTKE, ANDRZEJ · 2001 to 2016
$6.1M
NIA NIH HHS P01 AG031736NIA NIH HHS P01-AG031736NIA NIH HHS P30 AG013283NIA NIH HHS P30-AG013283NIA NIH HHS P30 AG024824NIA NIH HHS R01 AG019899NIA NIH HHS U01 AG022303
6 · The paper itself

Abstract

Work in yeast has shown that longevity extension induced by nutrient deprivation, altered ribosomal function, or diminished target of rapamycin action requires the activity of GCN4. We hypothesized that increased activity of ATF4, the mammalian equivalent of yeast GCN4, might be characteristic of mutations that extend mouse life span. Fibroblasts from the skin of two such mutants (Snell dwarf and PAPP-A knockout) were found to have higher levels of ATF4 protein and expression of several ATF4 target genes in responses to amino acid withdrawal, cadmium, hydrogen peroxide, and tunicamycin. ATF4 pathways were also elevated in liver of both kinds of long-lived mutant mice. Thus, a connection between ATF4 pathways and longevity may have deep evolutionary roots, and further studies of ATF4 mechanisms may provide insights into the links between cellular stress resistance, protein translation control, and aging.

Indexed as

Activating Transcription Factor 4AgingAnimalsCalcium ChannelsCell Culture TechniquesCell Cycle ProteinsFemaleFibroblastsLiverMiceMice, KnockoutPregnancy-Associated Plasma Protein-ARNA, MessengerSkinStress, PhysiologicalTranscription Factor CHOPActivating Transcription Factor 4Atf4 protein, mouseCalcium ChannelsCell Cycle ProteinsDdit3 protein, mousePregnancy-Associated Plasma Protein-ARNA, MessengerTranscription Factor CHOPTRB3 protein, mouseTrpv6 protein, mouseTRPV Cation ChannelsATF4Cell stress resistanceLife span.Slow aging

Identifiers

PMID24691093
PMCPMC4351389
OpenAlexW2105872446

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.