Evidence map›Paper›PMID 30952868›Full record

ArticleNature communications2019

Pellino1 regulates reversible ATM activation via NBS1 ubiquitination at DNA double-strand breaks.

Geun-Hyoung Ha, Jae-Hoon Ji, Sunyoung Chae, Jihyun Park, Suhyeon Kim, Jin-Kwan Lee, Yonghyeon Kim, Sunwoo Min, Jeong-Min Park, Tae-Hong Kang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-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

30 citing papers in PubMed, 47 citations in OpenAlex.

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  9. Potential promising of synthetic lethality in cancer research and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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  14. Article
  15. Ubiquitination Links DNA Damage and Repair Signaling to Cancer Metabolism.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. ATM: Functions of ATM Kinase and Its Relevance to Hereditary Tumors.International journal of molecular sciences · 2022
    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

13 authors at 5 institutions in 1 country.

Geun-Hyoung HaDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Jae-Hoon JiGenomic Instability Research Center, Ajou University School of Medicine, Suwon, 16499, Republic of Korea. jij@ajou.ac.kr.
Sunyoung ChaeInstitute of Medical Science, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Jihyun ParkDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, 06351, Republic of Korea.
Suhyeon KimDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Jin-Kwan LeeDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, 06351, Republic of Korea.
Yonghyeon KimDepartment of Biochemistry and Molecular Biology, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Sunwoo MinGenomic Instability Research Center, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Jeong-Min ParkDepartment of Biological Science, Dong-A University, Pusan, 49201, Republic of Korea.
Tae-Hong KangDepartment of Biological Science, Dong-A University, Pusan, 49201, Republic of Korea.
Ho LeeGraduate School of Cancer Science and Policy, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
Hyeseong ChoGenomic Instability Research Center, Ajou University School of Medicine, Suwon, 16499, Republic of Korea. hscho@ajou.ac.kr.
Chang-Woo LeeDepartment of Molecular Cell Biology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea. cwlee1234@skku.edu.
Ajou University · KRSungkyunkwan University · KRDong-A University · KRSamsung Medical Center · KRNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA double-strand break (DSB) signaling and repair are critical for genome integrity. They rely on highly coordinated processes including posttranslational modifications of proteins. Here we show that Pellino1 (Peli1) is a DSB-responsive ubiquitin ligase required for the accumulation of DNA damage response proteins and efficient homologous recombination (HR) repair. Peli1 is activated by ATM-mediated phosphorylation. It is recruited to DSB sites in ATM- and γH2AX-dependent manners. Interaction of Peli1 with phosphorylated histone H2AX enables it to bind to and mediate the formation of K63-linked ubiquitination of NBS1, which subsequently results in feedback activation of ATM and promotes HR repair. Collectively, these results provide a DSB-responsive factor underlying the connection between ATM kinase and DSB-induced ubiquitination.

Indexed as

DNA RepairAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorDNA Breaks, Double-StrandedHumansNuclear ProteinsUbiquitinationUbiquitin-Protein LigasesAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsNBN protein, humanNuclear ProteinsPELI1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID30952868
PMCPMC6450972
OpenAlexW2931817689

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.