ReviewCellular and molecular life sciences : CMLS2016
Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.
Review in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed, 122 citations in OpenAlex.
- FANCI promotes esophageal squamous cell carcinoma progression and cell cycle regulation and interacts with FANCD2.Journal of gastrointestinal oncology · 2026Article
- Fungal DNA damage repair: from model to driver of virulence and AMR.Bioscience reports · 2026Review
- DNA Polymerase Beta Catalytic and Fidelity Mutations Drive Platinum-Specific Drug Sensitivity.Cancers · 2026Article
- PARP4 ADP-ribosylates PIDD1 to complete a phospho/SUMO/PAR-ylation cascade that orchestrates PIDDosome assembly.Science advances · 2026Article
- Outcomes of patients with or without DNA repair pathway alterations: the MD Anderson IMPACT2 study.NPJ precision oncology · 2026Article
- Yeast Phenomic Analysis Reveals DNA Repair, pH Homeostasis, and Ribosomal Biogenesis as Modulators of Anticancer Ruthenium Complex KP1019.International journal of molecular sciences · 2026Article
- Current progress in research on ocular injury caused by exposure to vesicants.Progress in retinal and eye research · 2025Review
- Mechanistic insights into alcohol-induced DNA crosslink repair by Slx4-Xpf-Ercc1 nuclease complex in the Fanconi anaemia pathway.Communications biology · 2025Article
- Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.Orphanet journal of rare diseases · 2025Review
- Enhanced sensitivity, robust p21 activation, and sustained DNA repair responses to interstrand crosslinks in elephant cells compared to humans.Frontiers in veterinary science · 2025Article
- Multi-adductomics: Advancing mass spectrometry techniques for comprehensive exposome characterization.Trends in analytical chemistry : TRAC · 2024Article
- Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.PNAS nexus · 2024Article
- A minimal Fanconi Anemia complex in early diverging fungi.Scientific reports · 2024Article
- DoUBLing up: ubiquitin and ubiquitin-like proteases in genome stability.The Biochemical journal · 2024Review
- STIM1 translocation to the nucleus protects cells from DNA damage.Nucleic acids research · 2024Article
- Research progress on the fanconi anemia signaling pathway in non-obstructive azoospermia.Frontiers in endocrinology · 2024Review
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
- FIRRM cooperates with FIGNL1 to promote RAD51 disassembly during DNA repair.Science advances · 2023Article
- Phosphorylation by ATR triggers FANCD2 chromatin loading and activates the Fanconi anemia pathway.Cell reports · 2023Article
- KNO1-mediated autophagic degradation of the Bloom syndrome complex component RMI1 promotes homologous recombination.The EMBO journal · 2023Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Interstrand crosslinks (ICLs) are a highly toxic form of DNA damage. ICLs can interfere with vital biological processes requiring separation of the two DNA strands, such as replication and transcription. If ICLs are left unrepaired, it can lead to mutations, chromosome breakage and mitotic catastrophe. The Fanconi anemia (FA) pathway can repair this type of DNA lesion, ensuring genomic stability. In this review, we will provide an overview of the cellular response to ICLs. First, we will discuss the origin of ICLs, comparing various endogenous and exogenous sources. Second, we will describe FA proteins as well as FA-related proteins involved in ICL repair, and the post-translational modifications that regulate these proteins. Finally, we will review the process of how ICLs are repaired by both replication-dependent and replication-independent mechanisms.
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What OpenQuestion holds
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.