Rescuing the function of mutant p53
By A. Bullock, Alan R. Fersht. Nature Reviews. Cancer, 2001
608 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/68c2ea81418a6c5d3a649c76637d9ad1cd386017
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Citations in the corpus
- Apoptosis - the p53 network (2003, background): “Restoration of wild-type conformation to structurally contorted p53 DNA-binding mutants has been demonstrated, using peptide constructs and small molecular weight synthetic molecules (reviewed by Bullock and Fersht, 2001).”
- MicroRNA-21 targets a network of key tumor-suppressive pathways in glioblastoma cells. (2008, background): “The importance of p53 in preventing tumor formation is indicated by the presence of mutations in the p53 pathway in nearly all cancers (20).”
- When mutants gain new powers: news from the mutant p53 field (2009, background): “p53 bears the usual hallmarks of a transcription factor, with an amino-terminal transactivation domain, a core DNA-binding domain (DBD) and carboxy-terminal tetramerization and regulatory domain”
- Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis. (2011, background): “However, the vast majority of the mutations result in loss of p53’s ability to bind DNA in a sequence-specific manner and activate transcription of canonical p53 target genes.(12) TP53 mutations are distributed in all coding exons of the TP53 gene, with a strong predominance in exons 4-9, which enco”
- Cisplatin: mode of cytotoxic action and molecular basis of resistance (2003, background): “Thus, repair is intimately linked to checkpoint activation and apoptosis, and it is interesting that all three processes are collectively associated with the tumor-suppressor p53 protein (Morgan and Kastan, 1997; Bullock and Fersht, 2001).”