The DOI matches its Crossref record; 24 of the 25 references it cites were found in a registry or an index.
p73 is a human p53-related protein that can induce apoptosis
Abstract
The protein p53 is the most frequently mutated tumour suppressor to be identified so far in human cancers. The ability of p53 to inhibit cell growth is due, at least in part, to its ability to bind to specific DNA sequences and activate the transcription of target genes such as that encoding the cell-cycle inhibitor p21Waf1/Cip1 . A gene has recently been identified that is predicted to encode a protein with significant amino-acid sequence similarity to p53. In particular, each of the p53 amino-acid residues implicated in direct sequence-specific DNA binding is conserved in this protein. This gene, called p73, maps to the short arm of chromosome 1, and is found in a region that is frequently deleted in neuroblastomas. Here we show that p73 can, at least when overproduced, activate the transcription of p53-responsive genes and inhibit cell growth in a p53-like manner by inducing apoptosis (programmed cell death).
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In the citing paper
“p73 is a member of the p53 family of tumor suppressors and has similar transactivation functions relating to the induction of pro-apoptotic genes in response to cellular stress (17, 18).”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [17]
In the citing paper
“The p53 family member p73α has functions similar to p53 (17, 18, 42, 43), but is regulated differently by Mdm2.”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [17]
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Metadata
- Authors
- Jost, C. A., Marin, M. C., & Jr, W. G. K.
- Affiliations
- Harvard University (US)
- Venue
- Nature
- Published
- 1997-09-11
- Volume
- 389
- Issue
- 6647
- Pages
- 191-194
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1675096266
- Cited by
- 948
- References
- 25
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 13 · 2023: 7 · 2022: 15 · 2021: 18 · 2020: 13 · 2019: 13 · 2018: 11 · 2017: 15 · 2016: 18 · 2015: 20 · 2014: 19 · 2013: 25 · 2012: 26
- FWCI
- 34.25
- Type
- journal article
- Language
- en
- Update notices
- erratum (1999-06-24)
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- p73, p53, tumor suppressor proteins, apoptosis, transcriptional activation, cell growth inhibition, neuroblastoma, chromosome 1p deletion, p21, programmed cell death
- MeSH terms
- Tumor Protein p73, Cell Division, Cell Line, Chromosome Mapping, Chromosomes, Human, Pair 1, DNA-Binding Proteins, Growth Inhibitors, Humans, Molecular Sequence Data, Neuroblastoma, Nuclear Proteins, Plasmids, Tumor Cells, Cultured, Chloramphenicol O-Acetyltransferase, Transcriptional Activation, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Cyclins, Mutagenesis, Site-Directed, Apoptosis, Tumor Suppressor Proteins, Cyclin-Dependent Kinase Inhibitor p21
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