Evidence map›Paper›PMID 28797581›Full record

ReviewTrends in endocrinology and metabolism: TEM2017

Surviving Stress: Modulation of ATF4-Mediated Stress Responses in Normal and Malignant Cells.

Inge M N Wortel, Laurens T van der Meer, Michael S Kilberg, Frank N van Leeuwen

Open access · bronzeAbstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 380 papers.

0numbers the graph read from it
0cells of the map it votes in
380citing papers in PubMed
13.5field-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

380 citing papers in PubMed, 630 citations in OpenAlex.

  1. Article
  2. Preclinical evaluation of ixazomib for high-risk pediatric brain tumors.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Metabolomics Effects of Folding Correction in Retinitis Pigmentosa Rhodopsin Mutant P23A.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

320 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

4 authors at 3 institutions in 2 countries.

Inge M N WortelLaboratory of Pediatric Oncology, Radboud Institute for Molecular Life Science, Radboud university medical center, Nijmegen, The Netherlands; Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud university medical center, Nijmegen, The Netherlands.
Laurens T van der MeerLaboratory of Pediatric Oncology, Radboud Institute for Molecular Life Science, Radboud university medical center, Nijmegen, The Netherlands.
Michael S KilbergDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, FL 32610-0245, USA. Electronic address: mkilberg@ufl.edu.
Frank N van LeeuwenLaboratory of Pediatric Oncology, Radboud Institute for Molecular Life Science, Radboud university medical center, Nijmegen, The Netherlands. Electronic address: FrankN.vanLeeuwen@radboudumc.nl.
Radboud University Medical Center · NLFlorida College · USRadboud Institute for Molecular Life Sciences · NL

Funding

Nutritional Control of Cancer Cell Function by Amino AcidsR01CA203565 · NCI · UNIVERSITY OF FLORIDA · PI KILBERG, MICHAEL S. · 2015 to 2019
$1.7M
NCI NIH HHS R01 CA203565
6 · The paper itself

Abstract

Activating transcription factor 4 (ATF4) is a stress-induced transcription factor that is frequently upregulated in cancer cells. ATF4 controls the expression of a wide range of adaptive genes that allow cells to endure periods of stress, such as hypoxia or amino acid limitation. However, under persistent stress conditions, ATF4 promotes the induction of apoptosis. Recent advances point to a role for post-translational modifications (PTMs) and epigenetic mechanisms in balancing these pro- and anti-survival effects of ATF4. We review here how PTMs and epigenetic modifiers associated with ATF4 may be exploited by cancer cells to cope with cellular stress conditions that are intrinsically associated with tumor growth. Identification of mechanisms that modulate ATF4-mediated transcription and its effects on cellular metabolism may uncover new targets for cancer treatment.

Indexed as

Adaptation, PhysiologicalActivating Transcription Factor 4Amino AcidsAnimalsApoptosisCell SurvivalHumansHypoxiaNeoplasmsProtein Processing, Post-TranslationalStress, PhysiologicalActivating Transcription Factor 4Amino AcidsATF4 protein, humanATF4cellular stresspost-translational modification

Identifiers

PMID28797581
PMCPMC5951684
OpenAlexW2742971656

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.