Evidence map›Paper›PMID 28548464›Full record

ReviewThe FEBS journal2017

Control of cell death and mitochondrial fission by ERK1/2 MAP kinase signalling.

Simon J Cook, Kate Stuart, Rebecca Gilley, Matthew J Sale

Open access · hybridAbstract readReview
In one paragraph

Review in The FEBS journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% 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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Mitochondrial bioenergetics and networks in melanoma: an update.Apoptosis : an international journal on programmed cell death · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. Article

55 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 1 institution in 1 country.

Simon J CookSignalling Programme, The Babraham Institute, Cambridge, UK.ORCID 0000-0001-9087-1616
Kate StuartSignalling Programme, The Babraham Institute, Cambridge, UK.
Rebecca GilleySignalling Programme, The Babraham Institute, Cambridge, UK.
Matthew J SaleSignalling Programme, The Babraham Institute, Cambridge, UK.
Babraham Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BB/E02162X/1Biotechnology and Biological Sciences Research Council BB/L016397/1Biotechnology and Biological Sciences Research Council BBS/E/B/0000C199Biotechnology and Biological Sciences Research Council BBS/E/B/0000H151Biotechnology and Biological Sciences Research Council BBS/E/B/000C0413Biotechnology and Biological Sciences Research Council BBS/E/B/000C0417Biotechnology and Biological Sciences Research Council BBS/E/B/000C0419Cancer Research UK 14867Cancer Research UK A14867Worldwide Cancer Research 12-1259
6 · The paper itself

Abstract

The ERK1/2 signalling pathway is best known for its role in connecting activated growth factor receptors to changes in gene expression due to activated ERK1/2 entering the nucleus and phosphorylating transcription factors. However, active ERK1/2 also translocate to a variety of other organelles including the endoplasmic reticulum, endosomes, golgi and mitochondria to access specific substrates and influence cell physiology. In this article, we review two aspects of ERK1/2 signalling at the mitochondria that are involved in regulating cell fate decisions. First, we describe the prominent role of ERK1/2 in controlling the BCL2-regulated, cell-intrinsic apoptotic pathway. In most cases ERK1/2 signalling promotes cell survival by activating prosurvival BCL2 proteins (BCL2, BCL-x

Indexed as

Aniline CompoundsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisApoptosis Regulatory ProteinsBridged Bicyclo Compounds, HeterocyclicDrug Screening Assays, AntitumorHumansIndolesMAP Kinase Signaling SystemMitochondrial DynamicsMolecular Targeted TherapyNeoplasm ProteinsNeoplasmsOncogene AddictionProto-Oncogene Proteins c-bcl-2Aniline CompoundsApoptosis Regulatory ProteinsBridged Bicyclo Compounds, HeterocyclicIndolesnavitoclaxNeoplasm ProteinsobatoclaxPLX 4720Proto-Oncogene Proteins c-bcl-2PyrrolesSulfonamidesvenetoclaxapoptosisBCL2BH3-only proteinsBIMBRAFDRP1ERK1/2MEK1/2mitochondriaRAS

Identifiers

PMID28548464
PMCPMC6193418
OpenAlexW2617904586

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.