ArticleMolecular and cellular biology2004
DeltaNp73beta is active in transactivation and growth suppression.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 102 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
- TP73 Isoform-specific disruption reveals a critical role of TAp73beta in growth suppression and inflammatory response.Cell death & disease · 2023Article
- p73α1, a p73 C-terminal isoform, regulates tumor suppression and the inflammatory response via Notch1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- The p53 family member p73 in the regulation of cell stress response.Biology direct · 2021Review
- MDM2, MDMX, and p73 regulate cell-cycle progression in the absence of wild-type p53.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Tissue-specific expression of p73 and p63 isoforms in human tissues.Cell death & disease · 2021Article
- Review
- p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021Review
- The p53 Family: A Role in Lipid and Iron Metabolism.Frontiers in cell and developmental biology · 2021Review
- Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021Review
- Splicing machinery dysregulation drives glioblastoma development/aggressiveness: oncogenic role of SRSF3.Brain : a journal of neurology · 2020Article
- FDXR regulates TP73 tumor suppressor via IRP2 to modulate aging and tumor suppression.The Journal of pathology · 2020Article
- Article
- p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming.Cell death & disease · 2017Article
- Identification of two p53 isoforms from Litopenaeus vannamei and their interaction with NF-κB to induce distinct immune response.Scientific reports · 2017Article
- Alternative splicing and cell survival: from tissue homeostasis to disease.Cell death and differentiation · 2016Review
- p73 expression is regulated by ribosomal protein RPL26 through mRNA translation and protein stability.Oncotarget · 2016Article
- Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
p73, a p53 family protein, shares significant sequence homolog and functional similarity with p53. However, unlike p53, p73 has at least seven alternatively spliced isoforms with different carboxyl termini (p73alpha-eta). Moreover, the p73 gene can be transcribed from a cryptic promoter located in intron 3, producing seven more proteins (DeltaNp73alpha-eta). DeltaNp73, which does not contain the N-terminal activation domain in p73, has been thought to be transcriptionally inactive and dominant negative over p53 or p73. To systemically analyze the activity of the DeltaN variant, we generated stable cell lines, which inducibly express DeltaNp73alpha, DeltaNp73beta, and various DeltaNp73beta mutants by using the tetracycline-inducible expression system. Surprisingly, we found that DeltaNp73beta is indeed active in inducing cell cycle arrest and apoptosis. Importantly, we found that, when DeltaNp73beta is expressed at a physiologically relevant level, it is capable of suppressing cell growth. We then demonstrated that these DeltaNp73beta activities are not cell type specific. We showed that the 13 unique residues at the N terminus are required for DeltaNp73beta to suppress cell growth. We also found that, among the 13 residues, residues 6 to 10 are critical to DeltaNp73beta function. Furthermore, we found that DeltaNp73beta is capable of inducing some p53 target genes, albeit to a lesser extent than does p73beta. Finally, we found that the 13 unique residues, together with the N-terminal PXXP motifs, constitute a novel activation domain. Like DeltaNp73beta, DeltaNp73gamma is active in transactivation. However, unlike DeltaNp73beta, DeltaNp73alpha is inactive in suppressing cell growth. Our data, together with others' previous findings, suggest that DeltaNp73beta may have distinct functions under certain cellular circumstances.
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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.