Evidence map›Paper›PMID 39348153›Full record

ReviewThe FEBS journal2025

Atypical MAPKs in cancer.

Katrin Dahm, Parthiban Vijayarangakannan, Hans-Peter Wollscheid, Hansjörg Schild, Krishnaraj Rajalingam

Abstract readReview
In one paragraph

Review in The FEBS journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Integrated Network Pharmacology and Molecular Dynamics Reveal Luteolin fromInternational journal of molecular sciences · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
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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

5 authors.

Katrin DahmCell Biology Unit, University Medical Center Mainz, JGU-Mainz, Germany.
Parthiban VijayarangakannanSvastia Genetics, Future Business Centre, Cambridge, UK.
Hans-Peter WollscheidCell Biology Unit, University Medical Center Mainz, JGU-Mainz, Germany.
Hansjörg SchildInstitute of Immunology, University Medical Center Mainz, JGU-Mainz, Germany.
Krishnaraj RajalingamCell Biology Unit, University Medical Center Mainz, JGU-Mainz, Germany.ORCID 0000-0002-4175-9633

Funding

Deutsche Forschungsgemeinschaft CRC1272 (TP05)Deutsche Krebshilfe DKH 70113042
6 · The paper itself

Abstract

Impaired kinase signalling leads to various diseases, including cancer. At the same time, kinases make up the majority of the druggable genome and targeting kinase activity has proven to be a successful first-line therapy for many cancers. Among the best-studied kinases are the mitogen-activated protein kinases (MAPKs), which regulate cell proliferation, differentiation, motility, and survival. However, the MAPK family also contains the atypical members ERK3 (MAPK6), ERK4 (MAPK4), ERK7/ERK8 (MAPK15), and NLK that are functionally and structurally different from their conventional family members and have long been neglected. Nevertheless, in recent years, important roles in carcinogenesis, actin cytoskeleton regulation and the immune system have been discovered, underlining the physiological importance of atypical MAPKs and the need to better understand their functions. This review highlights the distinctive features of the atypical MAPKs and summarizes the evidence on their regulation, physiological roles, and potential targeting strategies for cancer therapies.

Indexed as

Mitogen-Activated Protein KinasesNeoplasmsAnimalsCell ProliferationHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinasescancer therapyERK3ERK4ERK7/8MAPK15MAPK4MAPK6Nemo‐like kinase

Identifiers

PMID39348153
PMCPMC12062777

What OpenQuestion holds

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Registered trials

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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.