ArticleProceedings of the National Academy of Sciences of the United States of America2007
RPA and ATR link transcriptional stress to p53.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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.
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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
65 citing papers in PubMed, 113 citations in OpenAlex.
- Nuclear-targeted GDOWN1 potently suppresses tumors by inducing premature transcription termination and exporting Pol Ⅱ CTD phosphatases to activate RB.Cell death and differentiation · 2026Article
- Targeting ATR-CHK1 and ATM-CHK2 Axes in Pancreatic Cancer-A Comprehensive Review of Literature.International journal of molecular sciences · 2026Review
- YTHDC1 mThe EMBO journal · 2024Article
- Integrator complex subunit 6 (INTS-6) mediates DNA damage response inmicroPublication biology · 2024Article
- Temozolomide, Procarbazine and Nitrosoureas in the Therapy of Malignant Gliomas: Update of Mechanisms, Drug Resistance and Therapeutic Implications.Journal of clinical medicine · 2023Review
- Requirement of transcription-coupled nucleotide excision repair for the removal of a specific type of oxidatively induced DNA damage.Nucleic acids research · 2023Article
- Competition for DNA binding between the genome protector replication protein A and the genome modifying APOBEC3 single-stranded DNA deaminases.Nucleic acids research · 2022Article
- Article
- ATR activity controls stem cell quiescence via the cyclin F-SCF complex.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- DNA folds threaten genetic stability and can be leveraged for chemotherapy.RSC chemical biology · 2021Review
- p53-GSDME Elevation: A Path for CDK7 Inhibition to Suppress Breast Cancer Cell Survival.Frontiers in molecular biosciences · 2021Article
- Article
- BRD4 prevents the accumulation of R-loops and protects against transcription-replication collision events and DNA damage.Nature communications · 2020Article
- Thirdhand smoke exposure causes replication stress and impaired transcription in human lung cells.Environmental and molecular mutagenesis · 2020Article
- ATR Kinase Activity Limits Mutagenesis and Promotes the Clonogenic Survival of Quiescent Human Keratinocytes Exposed to UVB Radiation.Photochemistry and photobiology · 2020Article
- ATR kinase inhibition sensitizes quiescent human cells to the lethal effects of cisplatin but increases mutagenesis.Mutation research · 2019Article
- Regulation of ATR activity via the RNA polymerase II associated factors CDC73 and PNUTS-PP1.Nucleic acids research · 2019Article
- Spironolactone Depletes the XPB Protein and Inhibits DNA Damage Responses in UVB-Irradiated Human Skin.The Journal of investigative dermatology · 2019Article
- Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.Environmental and molecular mutagenesis · 2018Review
- A novel role for ATR/Rad3 in G1 phase.Scientific reports · 2018Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms by which DNA-damaging agents trigger the induction of the stress response protein p53 are poorly understood but may involve alterations of chromatin structure or blockage of either transcription or replication. Here we show that transcription-blocking agents can induce phosphorylation of the Ser-15 site of p53 in a replication-independent manner. Furthermore, microinjection of anti-RNA polymerase II antibodies into the nuclei of cells showed that blockage of transcription is sufficient for p53 accumulation even in the absence of DNA damage. This induction of p53 occurs by two independent mechanisms. First, accumulation of p53 is linked to diminished nuclear export of mRNA; and second, inhibition specifically of elongating RNA polymerase II complexes results in the phosphorylation of the Ser-15 site of p53 in a replication protein A (RPA)- and ATM and Rad3-related (ATR)-dependent manner. We propose that this transcription-based stress response involving RPA, ATR, and p53 has evolved as a DNA damage-sensing mechanism to safeguard cells against DNA damage-induced mutagenesis.
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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.