ArticleCell cycle (Georgetown, Tex.)2009
Dissection of the sequence-specific DNA binding and exonuclease activities reveals a superactive yet apoptotically impaired mutant p53 protein.
Article in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Evaluation of non-canonical p53 functions in DNA replication and recombination for variant classification.Cell death & disease · 2026Article
- Canonical and non-canonical functions of p53 isoforms: potentiating the complexity of tumor development and therapy resistance.Cell death & disease · 2024Review
- The levels of p53 govern the hierarchy of DNA damage tolerance pathway usage.Nucleic acids research · 2024Article
- Exonucleases: Degrading DNA to Deal with Genome Damage, Cell Death, Inflammation and Cancer.Cells · 2022Review
- Synthetic lethality between TP53 and ENDOD1.Nature communications · 2022Article
- p53 isoforms differentially impact on the POLι dependent DNA damage tolerance pathway.Cell death & disease · 2021Article
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- The cancer-associated, gain-of-function TP53 variant P152Lp53 activates multiple signaling pathways implicated in tumorigenesis.The Journal of biological chemistry · 2019Article
- Review
- Genomic and metabolic characterization of a chromophobe renal cell carcinoma cell line model (UOK276).Genes, chromosomes & cancer · 2017Article
- 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
- Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Oncotarget · 2011Article
- Awakening guardian angels: drugging the p53 pathway.Nature reviews. Cancer · 2009Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Both sequence-specific DNA binding and exonuclease activities have been mapped to the central conserved core domain of p53. To gain more information about these two activities a series of mutants were generated that changed core domain histidine residues. Of these mutants, only one, H115N p53, showed markedly reduced exonuclease activity (ca. 15% of wild-type). Surprisingly, purified H115N p53 protein was found to be significantly more potent than wild-type p53 in binding to DNA by several criteria including gel mobility shift assay, filter binding and DNase I footprinting. Interestingly as well, non-specific DNA binding by the core domain of H115N p53 is superior to that of wild-type p53. To study H115N p53 in vivo, clones of H1299 cells expressing tetracycline regulated wild-type or H115N p53 were generated. H115N was both more potent than wild-type p53 in inducing p53 target genes such as p21 and PIG3 and was also more effective in arresting cells in G1. Unexpectedly, in contrast to wild-type p53, H115N p53 was markedly impaired in causing apoptosis when cells were subjected to DNA damage. Our results indicate that the exonuclease activity and transcriptional activation functions of p53 can be separated. They also extend previous findings showing that cell cycle arrest and apoptosis are separable functions of p53. Finally, these experiments confirm that DNA binding and xonuclease activities are distinct features of the p53 core domain.
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Registered trials
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