ArticleOncogene2000
p51A (TAp63gamma), a p53 homolog, accumulates in response to DNA damage for cell regulation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Common genetic variants on 3q28 contribute to non-small cell lung cancer susceptibility: evidence from 10 case-control studies.Molecular genetics and genomics : MGG · 2015Pooled it
- Non-coding genetic elements of lung cancer identified using whole genome sequencing in 13,722 Chinese.Nature communications · 2025Article
- TP63 Functions as a Tumor Suppressor Regulated by GAS5/miR-221-3p Signaling Axis in Human Non-Small Cell Lung Cancer Cells.Cancer management and research · 2023Article
- The dual role of p63 in cancer.Frontiers in oncology · 2023Review
- Article
- ECRG2, a novel transcriptional target of p53, modulates cancer cell sensitivity to DNA damage.Cell death & disease · 2020Article
- C-terminal α Domain of p63 Binds to p300 to Coactivate β-Catenin.Neoplasia (New York, N.Y.) · 2019Article
- A Decade of GWAS Results in Lung Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Review
- A Novel Hydroxamate-Based Compound WMJ-J-09 Causes Head and Neck Squamous Cell Carcinoma Cell Death via LKB1-AMPK-p38MAPK-p63-Survivin Cascade.Frontiers in pharmacology · 2018Article
- Improvement of gemcitabine sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 cells by RUNX2 depletion-mediated augmentation of TAp73-dependent cell death.Oncogenesis · 2016Article
- Lovastatin causes FaDu hypopharyngeal carcinoma cell death via AMPK-p63-survivin signaling cascade.Scientific reports · 2016Article
- Novel Implications of DNA Damage Response in Drug Resistance of Malignant Cancers Obtained from the Functional Interaction between p53 Family and RUNX2.Biomolecules · 2015Review
- Rare variants of large effect in BRCA2 and CHEK2 affect risk of lung cancer.Nature genetics · 2014Article
- Apoptosis-Related Single Nucleotide Polymorphisms and the Risk of Non-Small Cell Lung Cancer in Women.Journal of cancer therapeutics & research · 2014Article
- Quantitative assessment of the influence of TP63 gene polymorphisms and lung cancer risk: evidence based on 93,751 subjects.PloS one · 2014Article
- p63 is an alternative p53 repressor in melanoma that confers chemoresistance and a poor prognosis.The Journal of experimental medicine · 2013Article
- Role of p63 in Development, Tumorigenesis and Cancer Progression.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012Article
- TAp63γ enhances nucleotide excision repair through transcriptional regulation of DNA repair genes.DNA repair · 2012Article
- p63 is a suppressor of tumorigenesis and metastasis interacting with mutant p53.Cell death and differentiation · 2011Review
- Variation in TP63 is associated with lung adenocarcinoma in the UK population.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p51A, or TAp63gamma, a translation product of gene p51, or p63, was identified as a homolog of p53 in its primary structure and transactivating function. p53 plays a decision-making role in inducing either cell cycle arrest or apoptosis in response to DNA damage, and thereby preserves genome integrity of living cells. To compare the biological activities between p51A and p53, cell lines with low-level, constitutive expression of each protein were obtained by cDNA transfection of mouse erythroleukemic cells. Production of p51A with an apparent molecular mass of 57-kilodalton (kD) accompanied induction of p21waf1 and appearance of hemoglobin-producing cells. After DNA-damaging treatment either with ultraviolet light (UV) irradiation or with actinomycin D, the p51A protein accumulated in time courses corresponding to those of wild-type p53, and caused an increase in the hemoglobin-positive cell count. In contrast, p53-accumulated cells underwent apoptosis without exhibiting the feature of erythroid differentiation. The mode of p21waf1 and Bax-alpha upregulations varied between p51A- and p53-expressing cells and between the types of DNA damage. These results suggest the possibility that p51A induces differentiation under genotoxic circumstances. There may be cellular factors that control p51A protein stability and transactivating ability.
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