ArticleNucleic acids research2000
p53 C-terminal interaction with DNA ends and gaps has opposing effect on specific DNA binding by the core.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- p53 Binds Preferentially to Non-B DNA Structures Formed by the Pyrimidine-Rich Strands of GAA·TTC Trinucleotide Repeats Associated with Friedreich's Ataxia.Molecules (Basel, Switzerland) · 2019Article
- The C-terminal domain of p53 orchestrates the interplay between non-covalent and covalent poly(ADP-ribosyl)ation of p53 by PARP1.Nucleic acids research · 2018Article
- DOMMINO 2.0: integrating structurally resolved protein-, RNA-, and DNA-mediated macromolecular interactions.Database : the journal of biological databases and curation · 2016Article
- p53 Specifically Binds Triplex DNA In Vitro and in Cells.PloS one · 2016Article
- Preferential binding of hot spot mutant p53 proteins to supercoiled DNA in vitro and in cells.PloS one · 2013Article
- Transcriptional regulation by p53.Cold Spring Harbor perspectives in biology · 2010Review
- Dissection of the sequence-specific DNA binding and exonuclease activities reveals a superactive yet apoptotically impaired mutant p53 protein.Cell cycle (Georgetown, Tex.) · 2009Article
- Versatile functions of p53 protein in multicellular organisms.Biochemistry. Biokhimiia · 2007Review
- Human cytomegalovirus disrupts both ataxia telangiectasia mutated protein (ATM)- and ATM-Rad3-related kinase-mediated DNA damage responses during lytic infection.Journal of virology · 2007Article
- DNA bending by M.EcoKI methyltransferase is coupled to nucleotide flipping.Nucleic acids research · 2005Article
- Role of tumor suppressor p53 domains in selective binding to supercoiled DNA.Nucleic acids research · 2002Article
- Efficient specific DNA binding by p53 requires both its central and C-terminal domains as revealed by studies with high-mobility group 1 protein.Molecular and cellular biology · 2002Article
- p53 and recombination intermediates: role of tetramerization at DNA junctions in complex formation and exonucleolytic degradation.Oncogene · 2002Article
- The proline-rich domain of p53 is required for cooperation with anti-neoplastic agents to promote apoptosis of tumor cells.Oncogene · 2002Article
Corrections and comments
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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
In addition to binding DNA in a sequence-specific manner, the p53 tumour suppressor protein can interact with damaged DNA. In order to understand which structural features in DNA the C-teminal domain recognises we have studied the interaction of p53 protein with different types of DNA oligonucleotides imitating damaged DNA. Here we show that one unpaired nucleotide within double-stranded (ds)DNA is sufficient for recognition by the p53 C-terminus, either as a protruding end or as an internal gap in dsDNA. C-terminal interaction with DNA ends facilitated core domain binding to DNA, whereas interaction with gaps prevented core domain-DNA complexing, implying that p53 might adopt distinct conformations upon binding to different DNA lesions. These observations suggest that both single-strand and double-strand breaks can serve as a target for p53 C-terminal recognition in vivo and indicate that p53 might recruit different repair factors to the sites of damaged DNA depending on the type of lesion.
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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.