Evidence map›Paper›PMID 27446918›Full record

ReviewFrontiers in cell and developmental biology2016

Redundancy in the World of MAP Kinases: All for One.

Marc K Saba-El-Leil, Christophe Frémin, Sylvain Meloche

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–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

29 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Review
  14. ERK signalling: a master regulator of cell behaviour, life and fate.Nature reviews. Molecular cell biology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. MAPK/ERK Signaling in Regulation of Renal Differentiation.International journal of molecular sciences · 2019
    Review
  20. Article
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

3 authors.

Marc K Saba-El-LeilInstitute for Research in Immunology and Cancer, Université de Montréal Montréal, QC, Canada.
Christophe FréminInstitute for Research in Immunology and Cancer, Université de MontréalMontréal, QC, Canada; Institute for Research in Cancer of MontpellierMontpellier, France.
Sylvain MelocheInstitute for Research in Immunology and Cancer, Université de MontréalMontréal, QC, Canada; Molecular Biology Program, Université de MontréalMontréal, QC, Canada; Department of Pharmacology, Université de MontréalMontréal, QC, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protein kinases ERK1 and ERK2 are the effector components of the prototypical ERK1/2 mitogen-activated protein (MAP) kinase pathway. This signaling pathway regulates cell proliferation, differentiation and survival, and is essential for embryonic development and cellular homeostasis. ERK1 and ERK2 homologs share similar biochemical properties but whether they exert specific physiological functions or act redundantly has been a matter of controversy. However, recent studies now provide compelling evidence in support of functionally redundant roles of ERK1 and ERK2 in embryonic development and physiology. In this review, we present a critical assessment of the evidence for the functional specificity or redundancy of MAP kinase isoforms. We focus on the ERK1/ERK2 pathway but also discuss the case of JNK and p38 isoforms.

Indexed as

ERK1/2functional redundancyJNKMAP kinasesmouse geneticsp38signal transduction

Identifiers

PMID27446918
PMCPMC4921452

What OpenQuestion holds

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LicenceCC BY
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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.