ArticleNucleic acids research2008
TAp73beta and DNp73beta activate the expression of the pro-survival caspase-2S.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Dichotomous transactivation domains contribute to growth inhibitory and promotion functions of TAp73.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- DNp73 enhances tumor progression and immune evasion in multiple myeloma by targeting the MYC and MYCN pathways.Frontiers in immunology · 2024Article
- Mouse cortical organoids reveal key functions of p73 isoforms: TAp73 governs the establishment of the archetypical ventricular-like zones while DNp73 is central in the regulation of neural cell fate.Frontiers in cell and developmental biology · 2024Article
- Mechanisms of Survival of Cytomegalovirus-Infected Tumor Cells.Molecular biology · 2022Article
- Integrin β4 as a Potential Diagnostic and Therapeutic Tumor Marker.Biomolecules · 2021Review
- Review
- Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021Review
- Review
- The Role of Caspase-2 in Regulating Cell Fate.Cells · 2020Review
- p53-Related Transcription Targets of TAp73 in Cancer Cells-Bona Fide or Distorted Reality?International journal of molecular sciences · 2020Review
- Discovery, characterization and potential roles of a novel NF-YAx splice variant in human neuroblastoma.Journal of experimental & clinical cancer research : CR · 2019Article
- Melanoma cells resistant towards MAPK inhibitors exhibit reduced TAp73 expression mediating enhanced sensitivity to platinum-based drugs.Cell death & disease · 2018Article
- Integrin-β4 is a novel transcriptional target of TAp73.Cell cycle (Georgetown, Tex.) · 2018Article
- Article
- Interplay between TAp73 Protein and Selected Activator Protein-1 (AP-1) Family Members Promotes AP-1 Target Gene Activation and Cellular Growth.The Journal of biological chemistry · 2015Article
- ∆Np73 is capable of inducing apoptosis by co-ordinately activating several BH3-only proteins.Bioscience reports · 2015Article
- Hypoxia-inducible TAp73 supports tumorigenesis by regulating the angiogenic transcriptome.Nature cell biology · 2015Article
- Hypoxia-induced DNp73 stabilization regulates Vegf-A expression and tumor angiogenesis similar to TAp73.Cell cycle (Georgetown, Tex.) · 2015Article
- Suppression of acetylpolyamine oxidase by selected AP-1 members regulates DNp73 abundance: mechanistic insights for overcoming DNp73-mediated resistance to chemotherapeutic drugs.Cell death and differentiation · 2014Article
- Tailoring the models of transcription.International journal of molecular sciences · 2013Review
Corrections and comments
- Expression of concern
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p73, the p53 homologue, exists as a transactivation-domain-proficient TAp73 or deficient deltaN(DN)p73 form. Expectedly, the oncogenic DNp73 that is capable of inactivating both TAp73 and p53 function, is over-expressed in cancers. However, the role of TAp73, which exhibits tumour-suppressive properties in gain or loss of function models, in human cancers where it is hyper-expressed is unclear. We demonstrate here that both TAp73 and DNp73 are able to specifically transactivate the expression of the anti-apoptotic member of the caspase family, caspase-2(S). Neither p53 nor TAp63 has this property, and only the p73beta form, but not the p73alpha form, has this competency. Caspase-2 promoter analysis revealed that a non-canonical, 18 bp GC-rich Sp-1-binding site-containing region is essential for p73beta-mediated activation. However, mutating the Sp-1-binding site or silencing Sp-1 expression did not affect p73beta's transactivation ability. In vitro DNA binding and in vivo chromatin immunoprecipitation assays indicated that p73beta is capable of directly binding to this region, and consistently, DNA binding p73 mutant was unable to transactivate caspase-2(S). Finally, DNp73beta over-expression in neuroblastoma cells led to resistance to cell death, and concomitantly to elevated levels of caspase-2(S.) Silencing p73 expression in these cells led to reduction of caspase-2(S) expression and increased cell death. Together, the data identifies caspase-2(S) as a novel transcriptional target common to both TAp73 and DNp73, and raises the possibility that TAp73 may be over-expressed in cancers to promote survival.
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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.