Evidence map›Paper›PMID 33462414›Full record

ReviewCell death and differentiation2021

Roles and mechanisms of BAP1 deubiquitinase in tumor suppression.

Louis Masclef, Oumaima Ahmed, Benjamin Estavoyer, Bruno Larrivée, Nathalie Labrecque, Anastasia Nijnik, El Bachir Affar

Open access · greenAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
11.0field-weighted citation impact, top 1% 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

102 citing papers in PubMed, 182 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Regulation of ferroptosis by BAP1.Cell death and differentiation · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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  18. Computational Pipelines for Protein Ubiquitylation Analysis and Prediction.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  19. Article
  20. Article

42 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

7 authors at 2 institutions in 1 country.

Louis Masclef *Laboratory for Cell Signaling and Cancer, Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, H1T 2M4, Canada.ORCID http://orcid.org/0000-0003-3034-5758
Oumaima Ahmed *Laboratory for Cell Signaling and Cancer, Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, H1T 2M4, Canada.
Benjamin EstavoyerLaboratory for Cell Signaling and Cancer, Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, H1T 2M4, Canada.
Bruno LarrivéeLaboratory for Developmental and Pathological Angiogenesis, Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, H1T 2M4, Canada.
Nathalie LabrecqueLaboratory of Immunology, Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, H1T 2M4, Canada.
Anastasia NijnikMcGill University Research Centre on Complex Traits, Montreal, QC, H3G 0B1, Canada.
El Bachir AffarLaboratory for Cell Signaling and Cancer, Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, H1T 2M4, Canada. el.bachir.affar@umontreal.ca.ORCID http://orcid.org/0000-0002-6374-3683
Hôpital Maisonneuve-Rosemont · CAMcGill University · CA

Funding

CIHR
6 · The paper itself

Abstract

The BAP1 gene has emerged as a major tumor suppressor mutated with various frequencies in numerous human malignancies, including uveal melanoma, malignant pleural mesothelioma, clear cell renal cell carcinoma, intrahepatic cholangiocarcinoma, hepatocellular carcinoma, and thymic epithelial tumors. BAP1 mutations are also observed at low frequency in other malignancies including breast, colorectal, pancreatic, and bladder cancers. BAP1 germline mutations are associated with high incidence of mesothelioma, uveal melanoma, and other cancers, defining the "BAP1 cancer syndrome." Interestingly, germline BAP1 mutations constitute an important paradigm for gene-environment interactions, as loss of BAP1 predisposes to carcinogen-induced tumorigenesis. Inactivating mutations of BAP1 are also identified in sporadic cancers, denoting the importance of this gene for normal tissue homeostasis and tumor suppression, although some oncogenic properties have also been attributed to BAP1. BAP1 belongs to the deubiquitinase superfamily of enzymes, which are responsible for the maturation and turnover of ubiquitin as well as the reversal of substrate ubiquitination, thus regulating ubiquitin signaling. BAP1 is predominantly nuclear and interacts with several chromatin-associated factors, assembling multi-protein complexes with mutually exclusive partners. BAP1 exerts its function through highly regulated deubiquitination of its substrates. As such, BAP1 orchestrates chromatin-associated processes including gene expression, DNA replication, and DNA repair. BAP1 also exerts cytoplasmic functions, notably in regulating Ca

Indexed as

AnimalsCell DeathCell ProliferationGene-Environment InteractionGerm-Line MutationHumansNeoplasmsProtein Processing, Post-TranslationalTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1 protein, humanTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID33462414
PMCPMC7862696
OpenAlexW3124173816

What OpenQuestion holds

Textmetadata
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.