Evidence map›Paper›PMID 26680512›Full record

ArticleScientific reports2015

Cancer associated missense mutations in BAP1 catalytic domain induce amyloidogenic aggregation: A new insight in enzymatic inactivation.

Sushmita Bhattacharya, Pranita Hanpude, Tushar Kanti Maiti

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Phenotype-Specific Recalibration of MAVE Data Enables Repurposing ofmedRxiv : the preprint server for health sciences · 2026
    Article
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  5. Review
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  11. Clinical and molecular validation of BAP1, MTAP, P53, and Merlin immunohistochemistry in diagnosis of pleural mesothelioma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  12. Review
  13. Medical and Surgical Care of Patients With Mesothelioma and Their Relatives Carrying Germline BAP1 Mutations.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2022
    Review
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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

3 authors at 1 institution in 1 country.

Sushmita BhattacharyaLaboratory of Proteomics and Cellular Signaling, Regional Centre for Biotechnology, NCR Biotech Science Cluster, 3rd Milestone Gurgaon-Faridabad Expressway, Faridabad, Haryana 121001, INDIA.
Pranita HanpudeLaboratory of Proteomics and Cellular Signaling, Regional Centre for Biotechnology, NCR Biotech Science Cluster, 3rd Milestone Gurgaon-Faridabad Expressway, Faridabad, Haryana 121001, INDIA.
Tushar Kanti MaitiLaboratory of Proteomics and Cellular Signaling, Regional Centre for Biotechnology, NCR Biotech Science Cluster, 3rd Milestone Gurgaon-Faridabad Expressway, Faridabad, Haryana 121001, INDIA.
Regional Centre for Biotechnology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BRCA1 associated protein 1 (BAP1) is a nuclear deubiquitinase that regulates tumor suppressor activity and widely involves many cellular processes ranging from cell cycle regulation to gluconeogenesis. Impairment of enzymatic activity and nuclear localization induce abnormal cell proliferation. It is considered to be an important driver gene, which undergoes frequent mutations in several cancers. However the role of mutation and oncogenic gain of function of BAP1 are poorly understood. Here, we investigated cellular localization, enzymatic activity and structural changes for four missense mutants of the catalytic domain of BAP1, which are prevalent in different types of cancer. These mutations triggered cytoplasmic/perinuclear accumulation in BAP1 deficient cells, which has been observed in proteins that undergo aggregation in cellular condition. Amyloidogenic activity of mutant BAP1 was revealed from its reactivity towards anti oligomeric antibody in HEK293T cells. We have also noted structural destabilization in the catalytic domain mutants, which eventually produced beta amyloid structure as indicated in atomic force microscopy study. The cancer associated mutants up-regulate heat shock response and activates transcription of genes normally co-repressed by BAP1. Overall, our results unambiguously demonstrate that structural destabilization and subsequent aggregation abrogate its cellular mechanism leading to adverse outcome.

Indexed as

AmyloidCatalytic DomainCell Line, TumorCircular DichroismHeat-Shock ProteinsHEK293 CellsHumansMicroscopy, Atomic ForceMicroscopy, FluorescenceMutation, MissenseProtein StabilityProtein Structure, SecondaryTumor Suppressor ProteinsUbiquitin ThiolesteraseAmyloidBAP1 protein, humanHeat-Shock ProteinsTumor Suppressor ProteinsUbiquitin Thiolesterase

Identifiers

PMID26680512
PMCPMC4683529
OpenAlexW2219837350

What OpenQuestion holds

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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.