ArticleOncogene2002
p53 and recombination intermediates: role of tetramerization at DNA junctions in complex formation and exonucleolytic degradation.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- Homologous recombination defects and how they affect replication fork maintenance.AIMS genetics · 2018Review
- DNA damage tolerance pathway involving DNA polymerase ι and the tumor suppressor p53 regulates DNA replication fork progression.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Genetically defined subsets of human pancreatic cancer show unique in vitro chemosensitivity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Chromosome instability and deregulated proliferation: an unavoidable duo.Cellular and molecular life sciences : CMLS · 2012Review
- Article
- Relationship between VEGF and p53 expression and tumor cell proliferation in human gastrointestinal carcinomas.Journal of cancer research and clinical oncology · 2008Article
- Probing potential binding modes of the p53 tetramer to DNA based on the symmetries encoded in p53 response elements.Nucleic acids research · 2007Article
- Sequence analysis of p53 response-elements suggests multiple binding modes of the p53 tetramer to DNA targets.Nucleic acids research · 2007Article
- Wild-type p53 stimulates homologous recombination upon sequence-specific binding to the ribosomal gene cluster repeat.Oncogene · 2005Article
- DNA end joining becomes less efficient and more error-prone during cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- p53 protects from replication-associated DNA double-strand breaks in mammalian cells.Oncogene · 2004Article
- Poly(ADP-ribose) polymerase (PARP-1) and p53 independently function in regulating double-strand break repair in primate cells.Nucleic acids research · 2004Article
- p53 mutated in the transactivation domain retains regulatory functions in homology-directed double-strand break repair.Oncogene · 2003Article
- p53-associated 3'-->5' exonuclease activity in nuclear and cytoplasmic compartments of cells.Oncogene · 2003Article
- DNA substrate dependence of p53-mediated regulation of double-strand break repair.Molecular and cellular biology · 2002Article
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- Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heteroduplex joints represent intermediates of Rad51-dependent recombination processes, which are recognized by p53 with extremely high affinities, in a manner independent of the DNA sequence content. To determine the structural elements required for complex formation, we monitored DNA-binding by protection against restriction endonuclease cleavage. We show that wild-type (wt) p53 interacts with heteroduplex joints in the proximity of the flexible junction. Association of p53 within this junction region was also observed with preformed Rad51-heteroduplex complexes, whereas SSB counteracted p53 binding. At a distance of 31 bp from the junction p53 established very few contacts with the heteroduplex, despite the presence of an A-G mismatch. Consistently, p53-dependent exonucleolytic degradation decreased when we raised the distance between the junction and the heteroduplex terminus by 27 bp. Different from the cancer-related mutant p53(273H), which did not recognize the junction, tetramerization defective p53-1262 was protection competent but displayed reduced complex stability in gel shifts. Moreover, p53-1262 performed exonucleolytic activities towards ssDNA like wtp53, but reduced degradation of heteroduplex joints. These results suggest that during recombination wild-type p53, as a tetramer, stably binds to strand transfer regions, enabling the protein to exonucleolytically correct heteroduplex intermediates early after strand invasion.
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Registered trials
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