ArticleNucleic acids research2014
Damage-dependent regulation of MUS81-EME1 by Fanconi anemia complementation group A protein.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Prenatal Diagnosis of a Fetus With Congenital Malformations Caused by Compound Heterozygous Mutations in FANCA: A Case Report and Literature Review.Molecular genetics & genomic medicine · 2026Review
- Review
- Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021Review
- Fanconi anemia pathway as a prospective target for cancer intervention.Cell & bioscience · 2020Review
- Review
- Delineating the role of FANCA in glucose-stimulated insulin secretion in β cells through its protein interactome.PloS one · 2019Article
- FANCA Promotes DNA Double-Strand Break Repair by Catalyzing Single-Strand Annealing and Strand Exchange.Molecular cell · 2018Article
- Maintenance of genome stability by Fanconi anemia proteins.Cell & bioscience · 2017Review
- Cho Endonuclease Functions during DNA Interstrand Cross-Link Repair in Escherichia coli.Journal of bacteriology · 2016Article
- Human DNA Exonuclease TREX1 Is Also an Exoribonuclease That Acts on Single-stranded RNA.The Journal of biological chemistry · 2015Article
- Review
- Fanconi anemia signaling and Mus81 cooperate to safeguard development and crosslink repair.Nucleic acids research · 2014Article
- Human Fanconi anemia complementation group a protein stimulates the 5' flap endonuclease activity of FEN1.PloS one · 2013Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
MUS81-EME1 is a DNA endonuclease involved in replication-coupled repair of DNA interstrand cross-links (ICLs). A prevalent hypothetical role of MUS81-EME1 in ICL repair is to unhook the damage by incising the leading strand at the 3' side of an ICL lesion. In this study, we report that purified MUS81-EME1 incises DNA at the 5' side of a psoralen ICL residing in fork structures. Intriguingly, ICL repair protein, Fanconi anemia complementation group A protein (FANCA), greatly enhances MUS81-EME1-mediated ICL incision. On the contrary, FANCA exhibits a two-phase incision regulation when DNA is undamaged or the damage affects only one DNA strand. Studies using truncated FANCA proteins indicate that both the N- and C-moieties of the protein are required for the incision regulation. Using laser-induced psoralen ICL formation in cells, we find that FANCA interacts with and recruits MUS81 to ICL lesions. This report clarifies the incision specificity of MUS81-EME1 on ICL damage and establishes that FANCA regulates the incision activity of MUS81-EME1 in a damage-dependent manner.
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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.