ArticleNucleic acids research2016
Impaired TIP60-mediated H4K16 acetylation accounts for the aberrant chromatin accumulation of 53BP1 and RAP80 in Fanconi anemia pathway-deficient cells.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 78 citations in OpenAlex.
- SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA-PKcs/CHK1 replicative checkpoint to inhibit cell growth in non-small cell lung cancer.Molecular oncology · 2026Article
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
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- In silico protein structural analysis of PRMT5 and RUVBL1 mutations arising in human cancers.Cancer genetics · 2025Article
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- Intergenerational epigenetic inheritance mediated by MYS-2/MOF in the pathogenesis of Alzheimer's disease.iScience · 2024Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- Pathogenic effects of Leu200Pro and Arg387His VRK1 protein variants on phosphorylation targets and H4K16 acetylation in distal hereditary motor neuropathy.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Reversion from basal histone H4 hypoacetylation at the replication fork increases DNA damage in FANCA deficient cells.PloS one · 2024Article
- Chromodomain mutation in S. pombe Kat5/Mst1 affects centromere dynamics and DNA repair.PloS one · 2024Article
- Effects of Deacetylase Inhibition on the Activation of the Antioxidant Response and Aerobic Metabolism in Cellular Models of Fanconi Anemia.Antioxidants (Basel, Switzerland) · 2023Article
- Safeguarding DNA Replication: A Golden Touch of MiDAS and Other Mechanisms.International journal of molecular sciences · 2022Review
- Elevated RIF1 participates in the epigenetic abnormalities of zygotes by regulating histone modifications on MuERV-L in obese mice.Molecular medicine (Cambridge, Mass.) · 2022Article
- The multi-functionality of UHRF1: epigenome maintenance and preservation of genome integrity.Nucleic acids research · 2021Review
- Schizosaccharomyces pombe KAT5 contributes to resection and repair of a DNA double-strand break.Genetics · 2021Article
- Beyond DNA repair and chromosome instability-Fanconi anaemia as a cellular senescence-associated syndrome.Cell death and differentiation · 2021Review
- Methylation of histone 4's lysine 20: a critical analysis of the state of the field.Physiological genomics · 2021Review
- Identification of regulators of poly-ADP-ribose polymerase inhibitor response through complementary CRISPR knockout and activation screens.Nature communications · 2020Article
- VRK1 Phosphorylates Tip60/KAT5 and Is Required for H4K16 Acetylation in Response to DNA Damage.Cancers · 2020Article
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To rescue collapsed replication forks cells utilize homologous recombination (HR)-mediated mechanisms to avoid the induction of gross chromosomal abnormalities that would be generated by non-homologous end joining (NHEJ). Using DNA interstrand crosslinks as a replication barrier, we investigated how the Fanconi anemia (FA) pathway promotes HR at stalled replication forks. FA pathway inactivation results in Fanconi anemia, which is associated with a predisposition to cancer. FANCD2 monoubiquitination and assembly in subnuclear foci appear to be involved in TIP60 relocalization to the chromatin to acetylates histone H4K16 and prevents the binding of 53BP1 to its docking site, H4K20Me2. Thus, FA pathway loss-of-function results in accumulation of 53BP1, RIF1 and RAP80 at damaged chromatin, which impair DNA resection at stalled replication fork-associated DNA breaks and impede HR. Consequently, DNA repair in FA cells proceeds through the NHEJ pathway, which is likely responsible for the accumulation of chromosome abnormalities. We demonstrate that the inhibition of NHEJ or deacetylase activity rescue HR in FA cells.
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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.