ArticleProceedings of the National Academy of Sciences of the United States of America2020
DNA polymerase ι compensates for Fanconi anemia pathway deficiency by countering DNA replication stress.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Human TLS DNA polymerase: saviors or threats under replication stress?Molecular and cellular biochemistry · 2025Review
- Replication stress responses in human lymphocytes change sex-specifically during aging.Nucleic acids research · 2025Article
- E3 ubiquitin ligase RNF2 protects polymerase ι from destabilization.Biochimica et biophysica acta. Molecular cell research · 2024Article
- Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens.Nature reviews. Molecular cell biology · 2023Review
- Genome-wide siRNA screens identify RBBP9 function as a potential target in Fanconi anaemia-deficient head-and-neck squamous cell carcinoma.Communications biology · 2023Article
- PICKLES v3: the updated database of pooled in vitro CRISPR knockout library essentiality screens.Nucleic acids research · 2023Article
- Implications of Translesion DNA Synthesis Polymerases on Genomic Stability and Human Health.Molecular and cellular biology · 2023Article
- Dynamic rewiring of biological activity across genotype and lineage revealed by context-dependent functional interactions.Genome biology · 2022Article
- Review
- The emerging determinants of replication fork stability.Nucleic acids research · 2021Review
- Contracting eastern African CScientific reports · 2021Article
- When DNA Polymerases Multitask: Functions Beyond Nucleotidyl Transfer.Frontiers in molecular biosciences · 2021Review
- Fanconi Anemia Pathway Genes Advance Cervical CancerFrontiers in cell and developmental biology · 2021Article
- The Role of γH2AX in Replication Stress-induced Carcinogenesis: Possible Links and Recent Developments.Cancer diagnosis & prognosisReview
Corrections and comments
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
Abstract
Fanconi anemia (FA) is caused by defects in cellular responses to DNA crosslinking damage and replication stress. Given the constant occurrence of endogenous DNA damage and replication fork stress, it is unclear why complete deletion of FA genes does not have a major impact on cell proliferation and germ-line FA patients are able to progress through development well into their adulthood. To identify potential cellular mechanisms that compensate for the FA deficiency, we performed dropout screens in FA mutant cells with a whole genome guide RNA library. This uncovered a comprehensive genome-wide profile of FA pathway synthetic lethality, including
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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.