Evidence map›Paper›PMID 37387450›Full record

ReviewDisease models & mechanisms2023

CYLD in health and disease.

José L Marín-Rubio, Ishier Raote, Joseph Inns, Carol Dobson-Stone, Neil Rajan

Open access · goldAbstract readReview
In one paragraph

Review in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. [Ubiquitination-mediated regulation of T cell homeostasis and autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Role of CYLD in brain physiology and pathology.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  15. Review
  16. The CYLD-PARP1 feedback loop regulates DNA damage repair and chemosensitivity in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
  18. Frontiers in genetics · 2025
    Article
  19. 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

5 authors at 4 institutions in 3 countries.

José L Marín-RubioTranslational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.ORCID 0000-0002-7682-0190
Ishier RaoteUniversité de Paris, CNRS, Institut Jacques Monod, Paris 75016, France.ORCID 0000-0002-5898-4896
Joseph InnsTranslational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.ORCID 0000-0001-6761-4179
Carol Dobson-StoneBrain and Mind Centre and School of Medical Sciences, University of Sydney, Sydney, NSW 2050, Australia.ORCID 0000-0002-2211-0257
Neil RajanTranslational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.ORCID 0000-0002-5850-5680
Newcastle University · GBCentre National de la Recherche Scientifique · FRRoyal Victoria Infirmary · GBThe University of Sydney · AU

Funding

Department of Health
6 · The paper itself

Abstract

CYLD lysine 63 deubiquitinase (CYLD) is a ubiquitin hydrolase with important roles in immunity and cancer. Complete CYLD ablation, truncation and expression of alternate isoforms, including short CYLD, drive distinct phenotypes and offer insights into CYLD function in inflammation, cell death, cell cycle progression and cell transformation. Research in diverse model systems has shown that these are mediated via CYLD regulation of cellular pathways including the NF-κB, Wnt and TGF-β pathways. Recent biochemical advances and models have offered new insights into the regulation and function of CYLD. In addition, recent discoveries of gain-of-function germline pathogenic CYLD variants in patients with a neurodegenerative phenotype contrast with the more widely known loss-of-function mutations seen in patients with CYLD cutaneous syndrome and with sporadic cancers. Here, we provide a current review of mechanistic insights into CYLD function gained from CYLD animal models, as well as an update on the role of CYLD in human disease.

Indexed as

InflammationModels, BiologicalAnimalsCell DeathCell DivisionDeubiquitinating Enzyme CYLDHumansModels, AnimalCYLD protein, humanDeubiquitinating Enzyme CYLDCYLDCylindromaFrontotemporal dementiaGeneticsSkin tumoursUbiquitination

Identifiers

PMID37387450
PMCPMC10320722
OpenAlexW4382632016

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.