Evidence map›Paper›PMID 28622297›Full record

ArticleCell death and differentiation2017

p53-mediated suppression of BiP triggers BIK-induced apoptosis during prolonged endoplasmic reticulum stress.

Ignacio López, Anne-Sophie Tournillon, Rodrigo Prado Martins, Konstantinos Karakostis, Laurence Malbert-Colas, Karin Nylander, Robin Fåhraeus

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026
    Review
  2. Effects of GHRH and its analogues on the Vascular System.Reviews in endocrine & metabolic disorders · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Pathological implications of cellular stress in cardiovascular diseases.The international journal of biochemistry & cell biology · 2023
    Review
  11. Article
  12. Article
  13. DNA and RNA Binding Proteins: From Motifs to Roles in Cancer.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Virulence · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

7 authors at 4 institutions in 3 countries.

Ignacio LópezÉquipe Labellisée Ligue Contre le Cancer, Université Paris 7, INSERM UMR 1162 'Génomique Fonctionnelle des Tumeurs Solides', Paris, France.
Anne-Sophie TournillonÉquipe Labellisée Ligue Contre le Cancer, Université Paris 7, INSERM UMR 1162 'Génomique Fonctionnelle des Tumeurs Solides', Paris, France.
Rodrigo Prado MartinsÉquipe Labellisée Ligue Contre le Cancer, Université Paris 7, INSERM UMR 1162 'Génomique Fonctionnelle des Tumeurs Solides', Paris, France.
Konstantinos KarakostisÉquipe Labellisée Ligue Contre le Cancer, Université Paris 7, INSERM UMR 1162 'Génomique Fonctionnelle des Tumeurs Solides', Paris, France.
Laurence Malbert-ColasÉquipe Labellisée Ligue Contre le Cancer, Université Paris 7, INSERM UMR 1162 'Génomique Fonctionnelle des Tumeurs Solides', Paris, France.
Karin NylanderDepartment of Medical Biosciences; Umeå University, Umeå, Sweden.
Robin FåhraeusÉquipe Labellisée Ligue Contre le Cancer, Université Paris 7, INSERM UMR 1162 'Génomique Fonctionnelle des Tumeurs Solides', Paris, France.
Université Paris Cité · FRGénomique Fonctionnelle des Tumeurs Solides · FRInserm · FRUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Physiological and pathological conditions that affect the folding capacity of the endoplasmic reticulum (ER) provoke ER stress and trigger the unfolded protein response (UPR). The UPR aims to either restore the balance between newly synthesized and misfolded proteins or if the damage is severe, to trigger cell death. However, the molecular events underlying the switch between repair and cell death are not well understood. The ER-resident chaperone BiP governs the UPR by sensing misfolded proteins and thereby releasing and activating the three mediators of the UPR: PERK, IRE1 and ATF6. PERK promotes G2 cell cycle arrest and cellular repair by inducing the alternative translated p53 isoform p53ΔN40 (p53/47), which activates 14-3-3σ via suppression of p21

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisApoptosis Regulatory ProteinsCell Line, TumorEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesHeat-Shock ProteinsHumansMitochondrial ProteinsProtein Serine-Threonine KinasesTumor Suppressor Protein p53Unfolded Protein ResponseAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBik protein, mouseEndoplasmic Reticulum Chaperone BiPEndoribonucleasesHeat-Shock ProteinsMitochondrial ProteinsProtein Serine-Threonine KinasesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28622297
PMCPMC5596431
OpenAlexW2626186693

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.