ArticleOncogene2000
p53-dependent apoptosis is regulated by a C-terminally alternatively spliced form of murine p53.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- C-Terminal p53 Palindromic Tetrapeptide Restores Full Apoptotic Function to Mutant p53 Cancer Cells In Vitro and In Vivo.Biomedicines · 2023Article
- Changes in the expression of splicing factor transcripts and variations in alternative splicing are associated with lifespan in mice and humans.Aging cell · 2016Article
- p53 Isoforms: Key Regulators of the Cell Fate Decision.Cold Spring Harbor perspectives in medicine · 2016Review
- Biological functions of p53 isoforms through evolution: lessons from animal and cellular models.Cell death and differentiation · 2011Review
- p53 Isoforms: An Intracellular Microprocessor?Genes & cancer · 2011Article
- Inherited germline TP53 mutation encodes a protein with an aberrant C-terminal motif in a case of pediatric adrenocortical tumor.Familial cancer · 2011Article
- Transcriptomic and proteomic analyses of rhabdomyosarcoma cells reveal differential cellular gene expression in response to enterovirus 71 infection.Cellular microbiology · 2006Article
- p53 isoforms can regulate p53 transcriptional activity.Genes & development · 2005Article
- Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.Microbes and infection · 2005Article
- Having it both ways: transcription factors that bind DNA and RNA.Nucleic acids research · 2002Review
- DNA binding and 3'-5' exonuclease activity in the murine alternatively-spliced p53 protein.Oncogene · 2002Article
- The C-terminus of mutant p53 is necessary for its ability to interfere with growth arrest or apoptosis.Oncogene · 2001Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is now well accepted that the p53 C-terminus plays a central role in controlling the activity of the wild-type molecule. In our previous studies, we observed that a C-terminally altered p53 protein (p53AS), generated by an alternative spliced p53 mRNA, induces an attenuated p53-dependent apoptosis, compared to that induced by the regularly spliced form (p53RS). In the present study we analysed the interrelationships between these two physiological variants of wild-type p53, and found that in cells co-expressing both forms, in contrast to the expected additive effect on the induction of apoptosis, p53AS inhibits apoptosis induced by p53RS. This inhibitory effect is specific for p53-dependent apoptosis and was not evident in a p53-independent apoptotic pathway induced by growth factor deprivation. Furthermore, the expression of p53AS in transiently transfected cells caused both inhibition of apoptosis and inhibition of the p53RS-dependent transactivation of a number of p53 target genes. These results suggest that expression of an alternatively spliced p53 form may serve as an additional level in controlling the complexity of p53 function by the C-terminal domain.
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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.