ArticleCancer science2006
Identification of p53-46F as a super p53 with an enhanced ability to induce p53-dependent apoptosis.
Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Docetaxel plus trans-tracheal injection of adenoviral-mediated p53 versus docetaxel alone in patients with previously treated non-small-cell lung cancer.Cancer gene therapy · 2011Trial
- RNF144A and RNF144B: Important molecules for health.Open life sciences · 2025Review
- The Competition of Yin and Yang: Exploring the Role of Wild-Type and Mutant p53 in Tumor Progression.Biomedicines · 2023Article
- P63 and P73 Activation in Cancers with p53 Mutation.Biomedicines · 2022Review
- Roles of p53 Family Structure and Function in Non-Canonical Response Element Binding and Activation.International journal of molecular sciences · 2019Review
- Lysines in the tetramerization domain of p53 selectively modulate G1 arrest.Cell cycle (Georgetown, Tex.) · 2016Article
- High glucose dephosphorylates serine 46 and inhibits p53 apoptotic activity.Journal of experimental & clinical cancer research : CR · 2014Article
- The cell death machinery governed by the p53 tumor suppressor in response to DNA damage.Cancer science · 2010Review
- Stress-dependent Daxx-CHIP interaction suppresses the p53 apoptotic program.The Journal of biological chemistry · 2009Article
- Functional four-base A/T gap core sequence CATTAG of P53 response elements specifically bound tetrameric P53 differently than two-base A/T gap core sequence CATG bound both dimeric and tetrameric P53.Nucleic acids research · 2009Article
- Monomeric but not trimeric clathrin heavy chain regulates p53-mediated transcription.Oncogene · 2008Article
- von Willebrand factor type D domain mutant of SVS-1/SUSD2, vWD(m), induces apoptosis in HeLa cells.Cancer science · 2007Article
- The potential role of DFNA5, a hearing impairment gene, in p53-mediated cellular response to DNA damage.Journal of human genetics · 2006Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
More than half of human cancers contain mutations in the tumor suppressor protein p53, most of which accumulate in the DNA binding domain of the protein. Here we report the identification of a mutant p53, designated p53-46F, in which Ser-46 is replaced with phenylalanine. In vitro, adenovirus-mediated transduction of the p53-46F gene induced apoptosis more efficiently than wild-type p53 in a number of cancer cell lines, whereas Ser-15 phosphorylation of p53-46F was enhanced in all cancer cell lines examined. Moreover, the expression level of the cell cycle inhibitor p21/WAF1 was decreased in cell lines infected with adenovirus p53-46F (Ad-p53-46F). p53-46F caused a more enhanced level of transcriptional activation of several p53-target genes, including Noxa, p53AIP1 and p53RFP, compared with wild-type p53. In vivo, adenovirus-mediated gene transfer of p53-46F enhanced apoptosis, thus suppressing tumor growth of a lung cancer cell line more effectively than wild-type p53 or p53-121F, another p53 mutant. Collectively, our data suggest that p53-46F is an active version of p53 that demonstrates enhanced induction of p53-dependent apoptosis. This is probably mediated by upregulated transactivation of genes downstream of p53, increased Ser-15 phosphorylation and a decrease in p21/WAF1 levels. We propose p53-46F as an alternative candidate to wild-type p53 for use in developing new therapeutic strategies for the treatment of cancer.
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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.