Evidence map›Paper›PMID 34898277›Full record

ArticleMolecular and cellular biology2022

DNA Damage Triggers the Nuclear Accumulation of RASSF6 Tumor Suppressor Protein via CDK9 and BAF53 To Regulate p53 Target Gene Transcription.

Joshua Agbemefa Kuleape, Shakhawoat Hossain, Caleb Kwame Sinclear, Takanobu Shimizu, Hiroaki Iwasa, Junichi Maruyama, Kyoko Arimoto-Matsuzaki, Hiroshi Nishina, Yutaka Hata

Open access · greenAbstract read
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In one paragraph

Article in Molecular and cellular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 87% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. The Role of SWI/SNF Complex in Bladder Cancer.Journal of cellular and molecular medicine · 2025
    Review
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

9 authors at 1 institution in 2 countries.

Joshua Agbemefa KuleapeDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.
Shakhawoat HossainDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.
Caleb Kwame SinclearDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.
Takanobu ShimizuDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.
Hiroaki IwasaDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.ORCID 0000-0002-1994-2335
Junichi MaruyamaDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.ORCID 0000-0002-3665-2700
Kyoko Arimoto-MatsuzakiDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.ORCID 0000-0001-5485-8801
Hiroshi NishinaDepartment of Developmental and Regenerative Biology, Medical Research Institute, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.
Yutaka HataDepartment of Medical Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental Universitygrid.265073.5, Tokyo, Japan.ORCID 0000-0003-1304-5286
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RASSF6, a member of the tumor suppressor Ras-association domain family (RASSF) proteins, regulates cell cycle arrest and apoptosis via p53 and plays a tumor suppressor role. We previously reported that RASSF6 blocks MDM2-mediated p53 degradation and enhances p53 expression. In this study, we demonstrated that RASSF6 has nuclear localization and nuclear export signals and that DNA damage triggers the nuclear accumulation of RASSF6. We found that RASSF6 directly binds to BAF53, the component of SWI/SNF complex. DNA damage induces CDK9-mediated phosphorylation of BAF53, which enhances the interaction with RASSF6 and increases the amount of RASSF6 in the nucleus. Subsequently, RASSF6 augments the interaction between BAF53 and BAF60a, another component of the SWI/SNF complex, and further promotes the interaction of BAF53 and BAF60a with p53.

Indexed as

ActinsApoptosisApoptosis Regulatory ProteinsCell Cycle CheckpointsChromosomal Proteins, Non-HistoneCyclin-Dependent Kinase 9DNA-Binding ProteinsDNA DamageHumansMonomeric GTP-Binding ProteinsTranscription, GeneticTumor Suppressor Protein p53Tumor Suppressor ProteinsActinsACTL6A protein, humanApoptosis Regulatory ProteinsCDK9 protein, humanChromosomal Proteins, Non-HistoneCyclin-Dependent Kinase 9DNA-Binding ProteinsMonomeric GTP-Binding ProteinsRASSF6 protein, humanTumor Suppressor Protein p53Tumor Suppressor ProteinsapoptosisBAF53BAF60aCDK9p53RASSF6signal transductiontumor suppressor

Identifiers

PMID34898277
PMCPMC8852712
OpenAlexW4200273625

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.