ArticleNucleic acids research2003
Replication of damaged DNA in vitro is blocked by p53.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- Knockdown of CDK2AP1 in human embryonic stem cells reduces the threshold of differentiation.PloS one · 2018Article
- p53 in the DNA-Damage-Repair Process.Cold Spring Harbor perspectives in medicine · 2016Review
- Differential S-phase progression after irradiation of p53 functional versus non-functional tumour cells.Radiology and oncology · 2014Article
- Article
- Hbo1 Links p53-dependent stress signaling to DNA replication licensing.Molecular and cellular biology · 2008Article
- NMR chemical shift and relaxation measurements provide evidence for the coupled folding and binding of the p53 transactivation domain.Nucleic acids research · 2005Article
- The interaction of p53 with replication protein A mediates suppression of homologous recombination.Oncogene · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressor protein p53 may have other roles and functions in addition to its well-documented ability to serve as a sequence-specific transcriptional activator in response to DNA damage. We showed previously that p53 can block the replication of polyomavirus origin-containing DNA (Py ori-DNA) in vitro when p53 binding sites are present on the late side of the Py ori. Here we have both further extended these observations and have also examined whether p53 might be able to bind directly to and inhibit the replication of damaged DNA. We found that p53 strongly inhibits replication of gamma-irradiated Py ori-DNA and such inhibition requires both the central DNA binding domain and the extreme C-terminus of the p53 protein. An endogenous p53 binding site lies within the Py origin and is required for the ability of p53 to block initiation of replication from gamma-irradiated Py ori-DNA, suggesting the possibility of DNA looping caused by p53 binding both non-specifically to sites of DNA damage and specifically to the endogenous site in the polyomavirus origin. Our results thus suggest the possibility that under some circumstances p53 might serve as a direct regulator of DNA replication and suggest as well an additional function for cooperation between its two autonomous DNA binding domains.
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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 Socratic graph.