ArticleOncogene2003
Characterization of p73 functional domains necessary for transactivation and growth suppression.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 33 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
- Isoform-specific disruption of theeLife · 2023Article
- Article
- Review
- Review
- p73 expression is regulated by ribosomal protein RPL26 through mRNA translation and protein stability.Oncotarget · 2016Article
- Novel endogenous angiogenesis inhibitors and their therapeutic potential.Acta pharmacologica Sinica · 2015Review
- p53- and p73-independent activation of TIGAR expression in vivo.Cell death & disease · 2015Article
- An NF-κB p65-cIAP2 link is necessary for mediating resistance to TNF-α induced cell death in gliomas.Journal of neuro-oncology · 2011Article
- The G protein-coupled receptor 87 is necessary for p53-dependent cell survival in response to genotoxic stress.Cancer research · 2009Article
- Syntaxin 6, a regulator of the protein trafficking machinery and a target of the p53 family, is required for cell adhesion and survival.The Journal of biological chemistry · 2008Article
- DEC1, a basic helix-loop-helix transcription factor and a novel target gene of the p53 family, mediates p53-dependent premature senescence.The Journal of biological chemistry · 2008Article
- DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis.Journal of Zhejiang University. Science. B · 2007Review
- p53 and p73 display common and distinct requirements for sequence specific binding to DNA.Nucleic acids research · 2007Article
- RNPC1, an RNA-binding protein and a target of the p53 family, is required for maintaining the stability of the basal and stress-induced p21 transcript.Genes & development · 2006Article
- The C terminus of p53 family proteins is a cell fate determinant.Molecular and cellular biology · 2005Article
- DeltaNp73beta is active in transactivation and growth suppression.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
p73, a p53 family member, is highly similar to p53 in both structure and function. Like p53, the p73 protein contains an N-terminal activation domain, a DNA-binding domain, a tetramerization domain, and several PXXP motifs. Previously, we and others have shown that some functional domains in p53, such as the DNA-binding and tetramerization domains, are required for inducing both cell cycle arrest and apoptosis whereas others, such as the second activation domain, the proline-rich domain, and the C-terminal basic domain, are only required for inducing apoptosis. To determine the activity of p73 functional domains, we have generated stable inducible cell lines that express p73beta and various mutants deficient in one or more functional domains. We found that in addition to the DNA-binding domain, p73-mediated growth suppression requires the N-terminal activation domain and the tetramerization domain. However, unlike p53, p73-mediated apoptosis does not require the region adjacent to the activation domain or the entire C-terminal region. Interestingly, while the N- or the C-terminal PXXP motifs are dispensable for p73 function, deletion of both the N- and the C-terminal PXXP motifs renders p73 inactive in transactivation. In addition, we found that substitution of two conserved tandem hydrophobic residues with two hydrophilic ones, which can abrogate the activity of the first activation domain in p53, has no effect on p73 transcriptional activity. Together, we showed that the p73 protein has its own unique determinants for transactivation and growth suppression.
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.