Evidence map›Paper›PMID 27940552›Full record

ArticleNucleic acids research2017

And-1 coordinates with CtIP for efficient homologous recombination and DNA damage checkpoint maintenance.

Yali Chen, Hailong Liu, Haoxing Zhang, Changqing Sun, Zhaohua Hu, Qingsong Tian, Changmin Peng, Pei Jiang, Hui Hua, Xinzhi Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 29 citations in OpenAlex.

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  17. Heat KilledJournal of oncology · 2021
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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

11 authors at 3 institutions in 1 country.

Yali ChenState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Hailong LiuState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Haoxing ZhangSchool of Life Sciences and Oceanography, Shenzhen University, Shenzhen, Guangdong Province 518060, China.
Changqing SunDepartment of neurosurgery, Tianjin Baodi Hospital, Baodi Clinical College of Tianjin Medical University, Tianjin 301800, China.
Zhaohua HuDepartment of Orthopedics, Renhe Hospital of Three Gorges University, Yichang 443001, China.
Qingsong TianDepartment of Orthopedics, Renhe Hospital of Three Gorges University, Yichang 443001, China.
Changmin PengKey Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin Industrial Microbiology Key Lab, College of Biotechnology, Tianjin University of Science and Technology, No 29, 13ST. TEDA, Tianjin 300457, China.
Pei JiangState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Hui HuaState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Xinzhi LiDepartment of Orthopedics, Renhe Hospital of Three Gorges University, Yichang 443001, China.
Huadong PeiState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Beijing Proteome Research Center · CNChina Three Gorges University · CNTianjin University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To prevent genomic instability, cells respond to DNA lesions by blocking cell cycle progression and initiating DNA repair. Homologous recombination repair of DNA breaks requires CtIP-dependent resection of the DNA ends, which is thought to play a key role in activation of CHK1 kinase to induce the cell cycle checkpoint. But the mechanism is still not fully understood. Here, we establish that And-1, a replisome component, promotes DNA-end resection and DNA repair by homologous recombination. Mechanistically, And-1 interacts with CtIP and regulates CtIP recruitment to DNA damage sites. And-1 localizes to sites of DNA damage dependent on MDC1-RNF8 pathway, and is required for resistance to many DNA-damaging and replication stress-inducing agents. Furthermore, we show that And-1-CtIP axis is critically required for sustained ATR-CHK1 checkpoint signaling and for maintaining both the intra-S- and G2-phase checkpoints. Our findings thus identify And-1 as a novel DNA repair regulator and reveal how the replisome regulates the DNA damage induced checkpoint and genomic stability.

Indexed as

DNA DamageRecombinational DNA RepairCarrier ProteinsCell Cycle CheckpointsCell LineDNA-Binding ProteinsDNA ReplicationDNA, Single-StrandedEndodeoxyribonucleasesHumansNuclear ProteinsCarrier ProteinsDNA-Binding ProteinsDNA, Single-StrandedEndodeoxyribonucleasesNuclear ProteinsRBBP8 protein, humanWDHD1 protein, human

Identifiers

PMID27940552
PMCPMC5389581
OpenAlexW2566858108

What OpenQuestion holds

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LicenceCC BY-NC
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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.