Evidence map›Paper›PMID 36155803›Full record

ArticleNucleic acids research2022

SIAH2 regulates DNA end resection and replication fork recovery by promoting CtIP ubiquitination.

Seo-Yeon Jeong, Gurusamy Hariharasudhan, Min-Ji Kim, Ji-Yeon Lim, Sung Mi Jung, Eun-Ji Choi, In-Youb Chang, Younghoon Kee, Ho Jin You, Jung-Hee Lee

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
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

10 authors at 2 institutions in 1 country.

Seo-Yeon JeongLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
Gurusamy HariharasudhanLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
Min-Ji KimLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
Ji-Yeon LimLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
Sung Mi JungLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
Eun-Ji ChoiLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
In-Youb ChangDepartment of Anatomy, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.
Younghoon KeeDepartment of New Biology, Daegu Gyeongbuk Institute of Science and Technology (DGIST), 333 Techno-Joongang-daero, Dalseong-gun, Daegu 42988, Republic of Korea.
Ho Jin YouLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.ORCID 0000-0002-0530-4017
Jung-Hee LeeLaboratory of Genomic Instability and Cancer therapeutics, Chosun University School of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Republic of Korea.ORCID 0000-0002-6889-9126
Chosun University · KRDaegu Gyeongbuk Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human CtIP maintains genomic integrity primarily by promoting 5' DNA end resection, an initial step of the homologous recombination (HR). A few mechanisms have been suggested as to how CtIP recruitment to damage sites is controlled, but it is likely that we do not yet have full understanding of the process. Here, we provide evidence that CtIP recruitment and functioning are controlled by the SIAH2 E3 ubiquitin ligase. We found that SIAH2 interacts and ubiquitinates CtIP at its N-terminal lysine residues. Mutating the key CtIP lysine residues impaired CtIP recruitment to DSBs and stalled replication forks, DSB end resection, overall HR repair capacity of cells, and recovery of stalled replication forks, suggesting that the SIAH2-induced ubiquitination is important for relocating CtIP to sites of damage. Depleting SIAH2 consistently phenocopied these results. Overall, our work suggests that SIAH2 is a new regulator of CtIP and HR repair, and emphasizes that SIAH2-mediated recruitment of the CtIP is an important step for CtIP's function during HR repair.

Indexed as

DNA RepairDNA ReplicationCarrier ProteinsDNA Breaks, Double-StrandedEndodeoxyribonucleasesHumansNuclear ProteinsSeven in Absentia ProteinsUbiquitinationUbiquitin-Protein LigasesCarrier ProteinsEndodeoxyribonucleasesNuclear ProteinsRBBP8 protein, humanSeven in Absentia ProteinsUbiquitin-Protein Ligases

Identifiers

PMID36155803
PMCPMC9561274
OpenAlexW4297255296

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.