ArticleNature communications2022
The KU-PARP14 axis differentially regulates DNA resection at stalled replication forks by MRE11 and EXO1.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- CHK2 regulates MUS81-dependent DSBs in response to replication stress and BRCA2 deficiency.Nucleic acids research · 2026Article
- Structure, function, regulation, evolution, and therapeutic implications of PARP14.Genes & development · 2026Review
- Structural basis of Ku-mediated activation of WRN exonuclease activity.Nature communications · 2026Article
- Understanding single stranded DNA gaps: from formation to fate.The Biochemical journal · 2026Review
- The RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cells.NAR cancer · 2026Article
- The nuclease EXO1 promotes genomic instability by degrading nascent DNA in BRCA-proficient cells.Nature communications · 2026Article
- Genome-wide CRISPR screens identify the EXO1-CAF-1 pathway suppressing R-loop-associated DNA damage.Nucleic acids research · 2026Article
- Decoding replication stress responses through post-translational modifications.Nature chemical biology · 2025Review
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- PARP9-PARP13-PARP14 axis tunes colorectal cancer response to radiotherapy.Journal of experimental & clinical cancer research : CR · 2025Article
- The DNA-PKcs/JNK/p53 pathway underlies changes in cell fate decision toward death during DNA replication catastrophe.Nucleic acids research · 2025Article
- Targeting DNA damage sensors for cancer therapy.DNA repair · 2025Review
- ATM priming and end resection-coupled phosphorylation of MRE11 is important for fork protection and replication restart.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CRISPR knockout genome-wide screens identify the HELQ-RAD52 axis in regulating the repair of cisplatin-induced single-stranded DNA gaps.Nucleic acids research · 2024Article
- PARG inhibitor sensitivity correlates with accumulation of single-stranded DNA gaps in preclinical models of ovarian cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- PARP enzymes and mono-ADP-ribosylation: advancing the connection from interferon-signalling to cancer biology.Expert reviews in molecular medicine · 2024Review
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- PARP10 promotes the repair of nascent strand DNA gaps through RAD18 mediated translesion synthesis.Nature communications · 2024Article
- PARP14 is regulated by the PARP9/DTX3L complex and promotes interferon γ-induced ADP-ribosylation.The EMBO journal · 2024Article
- TCAF1 promotes TRPV2-mediated CaNature communications · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Suppression of nascent DNA degradation has emerged as an essential role of the BRCA pathway in genome protection. In BRCA-deficient cells, the MRE11 nuclease is responsible for both resection of reversed replication forks, and accumulation of single stranded DNA gaps behind forks. Here, we show that the mono-ADP-ribosyltransferase PARP14 is a critical co-factor of MRE11. PARP14 is recruited to nascent DNA upon replication stress in BRCA-deficient cells, and through its catalytic activity, mediates the engagement of MRE11. Loss or inhibition of PARP14 suppresses MRE11-mediated fork degradation and gap accumulation, and promotes genome stability and chemoresistance of BRCA-deficient cells. Moreover, we show that the KU complex binds reversed forks and protects them against EXO1-catalyzed degradation. KU recruits the PARP14-MRE11 complex, which initiates partial resection to release KU and allow long-range resection by EXO1. Our work identifies a multistep process of nascent DNA processing at stalled replication forks in BRCA-deficient cells.
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Registered trials
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.