ArticleProceedings of the National Academy of Sciences of the United States of America2022
Rapid recruitment of p53 to DNA damage sites directs DNA repair choice and integrity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- Variation at the R181 Residue of p53 Confers Loss of p53 DNA Binding Cooperativity with the Retention of Mitochondria-Associated Apoptosis.Molecular cancer research : MCR · 2026Article
- Phosphoinositides in membrane remodeling during infections and cellular stresses.FEBS letters · 2026Review
- Counteraction of HMGB1 at ss-dsDNA junctions maintains liquidity of protamine-DNA co-condensates.Nature communications · 2026Article
- Cigarette smoke induces FASN-dependent fatty acid metabolic rewiring to drive bladder cancer progression.Cancer letters · 2026Article
- Cell Type-Specific Expression of p16, p21, and p53 Reveals Age-Dependent Glial Senescence in the AppAging cell · 2026Article
- Multiomic single-cell perturbation screens reveal critical lncRNA regulators of senescence.Nature aging · 2026Article
- Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Investigating the functions and molecular mechanisms of DTX3L in cancer progression.Frontiers in oncology · 2026Review
- p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis.Frontiers in cell and developmental biology · 2026Review
- Specific TP53 mutations impair the recruitment of 53BP1 to DNA double-strand breaks underlying the mechanism of radioresistance.European biophysics journal : EBJ · 2025Article
- The E3 ubiquitin ligase DTX3L and the deubiquitinase USP28 fine-tune DNA repair through mutual regulation of their protein levels.iScience · 2025Article
- A cancer persistent DNA repair circuit driven by MDM2, MDM4 (MDMX), and mutant p53 for recruitment of MDC1 and 53BP1 on chromatin.Nucleic acids research · 2025Article
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025Review
- p53 enhances DNA repair and suppresses cytoplasmic chromatin fragments and inflammation in senescent cells.Nature communications · 2025Article
- p53-dependent chromatin relaxation is required for DNA double-strand break repair.Acta biochimica et biophysica Sinica · 2025Article
- A human-specific, concerted repression of microcephaly genes contributes to radiation-induced growth defects in cortical organoids.iScience · 2025Article
- Combination of ferulic acid and exercise alleviates menopause symptoms and skin remodeling in ovariectomized rats.Nutrition research and practice · 2025Article
- Linking signaling dynamics and cell fate decisions through single-cell imaging: evidence and challenges.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SignificanceOur work focuses on the critical longstanding question of the nontranscriptional role of p53 in tumor suppression. We demonstrate here that poly(ADP-ribose) polymerase (PARP)-dependent modification of p53 enables rapid recruitment of p53 to damage sites, where it in turn directs early repair pathway selection. Specifically, p53-mediated recruitment of 53BP1 at early time points promotes nonhomologous end joining over the more error-prone microhomology end-joining. Similarly, p53 directs nucleotide excision repair by mediating DDB1 recruitment. This property of p53 also correlates with tumor suppression in vivo. Our study provides mechanistic insight into how certain transcriptionally deficient p53 mutants may retain tumor-suppressive functions through regulating the DNA damage response.
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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.