ArticleNature communications2017
Parallel genome-wide screens identify synthetic viable interactions between the BLM helicase complex and Fanconi anemia.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
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- HAP1, a new revolutionary cell model for gene editing using CRISPR-Cas9.Frontiers in cell and developmental biology · 2023Review
- Nuclear export restricts Gdown1 to a mitotic function.Nucleic acids research · 2022Article
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- RecQ Helicase Somatic Alterations in Cancer.Frontiers in molecular biosciences · 2022Review
- EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart.Molecular cell · 2021Article
- SLFN11 promotes stalled fork degradation that underlies the phenotype in Fanconi anemia cells.Blood · 2021Article
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- Genome-scale CRISPR screening at high sensitivity with an empirically designed sgRNA library.BMC biology · 2020Article
- High-throughput synthetic rescue for exhaustive characterization of suppressor mutations in human genes.Cellular and molecular life sciences : CMLS · 2020Review
- Distinct roles of BRCA2 in replication fork protection in response to hydroxyurea and DNA interstrand cross-links.Genes & development · 2020Article
- Genetic interaction mapping and exon-resolution functional genomics with a hybrid Cas9-Cas12a platform.Nature biotechnology · 2020Article
- Systematic functional identification of cancer multi-drug resistance genes.Genome biology · 2020Article
- ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres.Nucleus (Austin, Tex.) · 2019Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 4 countries.
Funding
Abstract
Maintenance of genome integrity via repair of DNA damage is a key biological process required to suppress diseases, including Fanconi anemia (FA). We generated loss-of-function human haploid cells for FA complementation group C (FANCC), a gene encoding a component of the FA core complex, and used genome-wide CRISPR libraries as well as insertional mutagenesis to identify synthetic viable (genetic suppressor) interactions for FA. Here we show that loss of the BLM helicase complex suppresses FANCC phenotypes and we confirm this interaction in cells deficient for FA complementation group I and D2 (FANCI and FANCD2) that function as part of the FA I-D2 complex, indicating that this interaction is not limited to the FA core complex, hence demonstrating that systematic genome-wide screening approaches can be used to reveal genetic viable interactions for DNA repair defects.
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Registered trials
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