ArticleNature communications2016
p53 downregulates the Fanconi anaemia DNA repair pathway.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.Cell death and differentiation · 2026Article
- UBE2T-Mediated HP1α Ubiquitination Enhances Nucleolar Function and Promotes the Progression of IDH1/TP53-Mutant Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.PLoS computational biology · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.bioRxiv : the preprint server for biology · 2025Article
- Development of translational read-through-inducing drugs as novel therapeutic options for patients with Fanconi anemia.Cell death discovery · 2025Article
- Inhibition of the STAT3/Fanconi anemia axis is synthetic lethal with PARP inhibition in breast cancer.Nature communications · 2025Article
- Enhanced sensitivity, robust p21 activation, and sustained DNA repair responses to interstrand crosslinks in elephant cells compared to humans.Frontiers in veterinary science · 2025Article
- Ultrarare Variants in DNA Damage Repair Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome or Acute Behavioral Regression in Neurodevelopmental Disorders.Developmental neuroscience · 2025Article
- Identifying an AML Prognostic Model Using 10 Marker Genes from Single-Cell Transcriptome and Bulk Transcriptome Analysis.Biochemical genetics · 2024Article
- The Compromised Fanconi Anemia Pathway in Prelamin A-Expressing Cells Contributes to Replication Stress-Induced Genomic Instability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mutant p53 reactivation restricts the protumorigenic consequences of wild type p53 loss of heterozygosity in Li-Fraumeni syndrome patient-derived fibroblasts.Cell death and differentiation · 2024Article
- Targeting FBXO22 enhances radiosensitivity in non-small cell lung cancer by inhibiting the FOXM1/Rad51 axis.Cell death & disease · 2024Article
- Effects of p53 and ATRX inhibition on telomeric recombination in aging fibroblasts.Frontiers in oncology · 2024Article
- Modified iPOND revealed the role of mutant p53 in promoting helicase function and telomere maintenance.Aging · 2023Article
- p53 in the Molecular Circuitry of Bone Marrow Failure Syndromes.International journal of molecular sciences · 2023Review
- Gene therapy restores the transcriptional program of hematopoietic stem cells in Fanconi anemia.Haematologica · 2023Article
- A systematic approach identifies p53-DREAM pathway target genes associated with blood or brain abnormalities.Disease models & mechanisms · 2023Article
- The p53 DNA damage response and Fanconi anemia DNA repair pathway protect against acetaldehyde-induced replication stress in esophageal keratinocytes.Cell cycle (Georgetown, Tex.) · 2023Article
- RNF4 and USP7 cooperate in ubiquitin-regulated steps of DNA replication.Open biology · 2023Article
- Fanconi anemia pathway regulation by FANCI in prostate cancer.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Germline mutations affecting telomere maintenance or DNA repair may, respectively, cause dyskeratosis congenita or Fanconi anaemia, two clinically related bone marrow failure syndromes. Mice expressing p53(Δ31), a mutant p53 lacking the C terminus, model dyskeratosis congenita. Accordingly, the increased p53 activity in p53(Δ31/Δ31) fibroblasts correlated with a decreased expression of 4 genes implicated in telomere syndromes. Here we show that these cells exhibit decreased mRNA levels for additional genes contributing to telomere metabolism, but also, surprisingly, for 12 genes mutated in Fanconi anaemia. Furthermore, p53(Δ31/Δ31) fibroblasts exhibit a reduced capacity to repair DNA interstrand crosslinks, a typical feature of Fanconi anaemia cells. Importantly, the p53-dependent downregulation of Fanc genes is largely conserved in human cells. Defective DNA repair is known to activate p53, but our results indicate that, conversely, an increased p53 activity may attenuate the Fanconi anaemia DNA repair pathway, defining a positive regulatory feedback loop.
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