ArticleOncogene2001
P53 plays a protective role against UV- and cisplatin-induced apoptosis in transcription-coupled repair proficient fibroblasts.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 98 citations in OpenAlex.
- Article
- Role of Cockayne Syndrome Group B Protein in Replication Stress: Implications for Cancer Therapy.International journal of molecular sciences · 2022Review
- Hrq1/RECQL4 regulation is critical for preventing aberrant recombination during DNA intrastrand crosslink repair and is upregulated in breast cancer.PLoS genetics · 2022Article
- Current and emerging roles of Cockayne syndrome group B (CSB) protein.Nucleic acids research · 2021Review
- Review
- Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine.PloS one · 2020Article
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
- Comparison of responsiveness to cancer development and anti-cancer drug in three different C57BL/6N stocks.Laboratory animal research · 2019Article
- Base and nucleotide excision repair facilitate resolution of platinum drugs-induced transcription blockage.Nucleic acids research · 2018Article
- Article
- Guanidine Alkaloids from the Marine Sponge Monanchora pulchra Show Cytotoxic Properties and Prevent EGF-Induced Neoplastic Transformation in Vitro.Marine drugs · 2016Article
- The Stress-responsive Gene ATF3 Mediates Dichotomous UV Responses by Regulating the Tip60 and p53 Proteins.The Journal of biological chemistry · 2016Article
- DNA damage response (DDR) pathway engagement in cisplatin radiosensitization of non-small cell lung cancer.DNA repair · 2016Article
- Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome.Journal of molecular biology · 2016Article
- The role of peroxisome proliferator-activated receptor-coactivator-1 gene in skin aging.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2016Review
- Transcription Blockage Leads to New Beginnings.Biomolecules · 2015Review
- Transcriptional and post-transcriptional regulation of nucleotide excision repair genes in human cells.Mutation research · 2015Article
- DNA repair mechanisms in cancer development and therapy.Frontiers in genetics · 2015Article
- CSB interacts with SNM1A and promotes DNA interstrand crosslink processing.Nucleic acids research · 2015Article
- Reprogramming the mechanism of action of chlorambucil by coupling to a G-quadruplex ligand.Journal of the American Chemical Society · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
We previously reported that transcription-coupled repair (TCR)-deficient human fibroblasts are extremely sensitive to UV-induced apoptosis and this sensitivity correlated with the induction of the p53 tumour suppressor. However, we have also found that p53 can be protective against UV-induced apoptosis. Thus, prior to this study, it was not clear whether the induction of p53 in TCR-deficient fibroblasts contributed to their death. To address this issue, we have expressed human papillomavirus E6 (HPV-E6) in primary fibroblasts derived from patients affected with xeroderma pigmentosum (complementation groups A, B and C) and Cockayne syndrome (complementation group B). We found that TCR-deficient (XP-A, XP-B and CS-B) fibroblasts were more sensitive than TCR-proficient cells (XP-C and normal) to both UV light and cisplatin treatment and this increase in sensitivity was not p53 dependent. Importantly, HPV-E6 expression increased the sensitivity of TCR-proficient normal and XP-C fibroblasts to UV- and cisplatin-induced apoptosis. This increase in sensitivity correlated with a decrease in the capacity of HPV-E6 expressing cells to recover mRNA synthesis following UV-irradiation. Therefore, we propose that p53 protects against UV- and cisplatin-induced apoptosis in a TCR-dependent manner and that p53 does not contribute strongly to the induction of apoptosis in TCR-deficient fibroblasts.
Indexed as
Identifiers
What OpenQuestion holds
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.