Restoring the guardian of the genome

The unmutated, or wild-type, version of the gene, which was cloned from humans and mice in the 1980s, exerted the exact opposite effect: the gene acted as a potent inhibitor of tumorigenesis (S. J. Baker et al. Environmental stress, abnormal metabolic activity, genetic damage and advanced ageing can...

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Bibliographic Details
Published inNature (London) Vol. 603; no. 7899; p. S1
Main Author Eisenstein, Michael
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group 03.03.2022
Subjects
Aging
Cancer
Cell death
Chromosome aberrations
Cloning
Environmental stress
Gene expression
Genomes
Li-Fraumeni syndrome
Molecular weight
Mutation
p53 Protein
Proteins
Tumorigenesis
Tumors
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Summary:The unmutated, or wild-type, version of the gene, which was cloned from humans and mice in the 1980s, exerted the exact opposite effect: the gene acted as a potent inhibitor of tumorigenesis (S. J. Baker et al. Environmental stress, abnormal metabolic activity, genetic damage and advanced ageing can all trigger the protein's activation, enabling p53 to directly regulate the expression of hundreds of genes to initiate an appropriate response. Cell Death Differ. 25, 154-160; 2018), and nearly 90% of people born with such mutations - a rare hereditary condition known as Li-Fraumeni Syndrome - will develop cancer in their lifetime.
ISSN:0028-0836
1476-4687
DOI:10.1038/d41586-022-00565-x