Evidence map›Paper›PMID 27698029›Full record

ReviewCold Spring Harbor perspectives in biology2016

Cell Signaling and Stress Responses.

Gökhan S Hotamisligil, Roger J Davis

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
297citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

297 citing papers in PubMed, 1 synthesis or guideline pooled it, 488 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. Temporal Interference Stimulation Enhances Neural Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  10. Article
  11. The E3 Ligase RNF8 Promotes Ubiquitination and Degradation of ChREBPα During Liver Stress Response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Mutually exclusive alternative pre-mRNA splicing promotes adaptive metabolic stress signaling by JNK.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  16. Comprehensive analysis of the potential role of Ferroptosis-related genes in glioblastoma multiforme.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  17. Review
  18. Article
  19. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  20. Article

237 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

2 authors at 2 institutions in 1 country.

Gökhan S HotamisligilDepartment of Genetics and Complex Diseases, Broad Institute of Harvard-MIT, Harvard School of Public Health, Boston, Massachusetts 02115.
Roger J DavisHoward Hughes Medical Institute and Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605.
Broad Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress-signaling pathways are evolutionarily conserved and play an important role in the maintenance of homeostasis. These pathways are also critical for adaptation to new cellular environments. The endoplasmic reticulum (ER) unfolded protein response (UPR) is activated by biosynthetic stress and leads to a compensatory increase in ER function. The JNK and p38 MAPK signaling pathways control adaptive responses to intracellular and extracellular stresses, including environmental changes such as UV light, heat, and hyperosmotic conditions, and exposure to inflammatory cytokines. Metabolic stress caused by a high-fat diet represents an example of a stimulus that coordinately activates both the UPR and JNK/p38 signaling pathways. Chronic activation of these stress-response pathways ultimately causes metabolic changes associated with obesity and altered insulin sensitivity. Stress-signaling pathways, therefore, represent potential targets for therapeutic intervention in the metabolic stress response and other disease processes.

Indexed as

Oxidative StressSignal TransductionAnimalsHumansMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesUnfolded Protein Responsep38 Mitogen-Activated Protein Kinases

Identifiers

PMID27698029
PMCPMC5046695
OpenAlexW2528851536

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.