Evidence map›Paper›PMID 26781088›Full record

ArticleNature communications2016

TRAIP/RNF206 is required for recruitment of RAP80 to sites of DNA damage.

Nam Soo Lee, Hee Jin Chung, Hyoung-June Kim, Seo Yun Lee, Jae-Hoon Ji, Yoojeong Seo, Seung Hun Han, Minji Choi, Miyong Yun, Seok-Geun Lee and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. DOT1L-mediated RAP80 methylation promotes BRCA1 recruitment to elicit DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Review
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  15. Saudi journal of biological sciences · 2021
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  16. Article
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  18. CUL2EMBO reports · 2021
    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

14 authors at 5 institutions in 1 country.

Nam Soo LeeDepartment of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Hee Jin ChungDepartment of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Hyoung-June KimDepartment of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Seo Yun LeeGenomic Instability Research Center, Ajou University School of Medicine, Suwon 16499, Korea.
Jae-Hoon JiGenomic Instability Research Center, Ajou University School of Medicine, Suwon 16499, Korea.
Yoojeong SeoDepartment of Biological Sciences, Sookmyung Women's University, Seoul 04310, Republic of Korea.
Seung Hun HanDepartment of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Minji ChoiDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
Miyong YunDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
Seok-Geun LeeDepartment of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
Kyungjae MyungCenter for Genomic Integrity, Institute for Basic Science (IBS), Ulsan National Institute of Science and Technology, Ulsan 44919, Korea.
Yonghwan KimDepartment of Biological Sciences, Sookmyung Women's University, Seoul 04310, Republic of Korea.
Ho Chul KangGenomic Instability Research Center, Ajou University School of Medicine, Suwon 16499, Korea.
Hongtae KimDepartment of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Sungkyunkwan University · KRAjou University · KRKyung Hee University · KRSookmyung Women's University · KRInstitute for Basic Science · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RAP80 localizes to sites of DNA insults to enhance the DNA-damage responses. Here we identify TRAIP/RNF206 as a novel RAP80-interacting protein and find that TRAIP is necessary for translocation of RAP80 to DNA lesions. Depletion of TRAIP results in impaired accumulation of RAP80 and functional downstream partners, including BRCA1, at DNA lesions. Conversely, accumulation of TRAIP is normal in RAP80-depleted cells, implying that TRAIP acts upstream of RAP80 recruitment to DNA lesions. TRAIP localizes to sites of DNA damage and cells lacking TRAIP exhibit classical DNA-damage response-defect phenotypes. Biochemical analysis reveals that the N terminus of TRAIP is crucial for RAP80 interaction, while the C terminus of TRAIP is required for TRAIP localization to sites of DNA damage through a direct interaction with RNF20-RNF40. Taken together, our findings demonstrate that the novel RAP80-binding partner TRAIP regulates recruitment of the damage signalling machinery and promotes homologous recombination.

Indexed as

Carrier ProteinsCell Line, TumorCell SurvivalDNA-Binding ProteinsDNA DamageHEK293 CellsHeLa CellsHistone ChaperonesHumansImmunoprecipitationIn Vitro TechniquesNuclear ProteinsProtein BindingProtein TransportTissue Array AnalysisTwo-Hybrid System TechniquesCarrier ProteinsDNA-Binding ProteinsHistone ChaperonesNuclear ProteinsTRAIP protein, humanUbiquitin-Protein LigasesUIMC1 protein, human

Identifiers

PMID26781088
PMCPMC4735692
OpenAlexW2268274178

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.