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'Checkpoint' controls arrest the cell cycle after DNA damage, allowing repair to take place before mutations can be perpetuated. In multicellular organisms, DNA damage can also induce apoptotic cell death, protecting the organism at the expense of the individual cell. How does a cell 'choose' between cycle arrest and death? Analysis of two human tumour suppressor proteins, p53 and the ATM (ataxia-telangiectasia mutated) gene product, may provide some answers.

Type

Journal article

Journal

Trends Biochem Sci

Publication Date

10/1995

Volume

20

Pages

426 - 430

Keywords

Apoptosis, Ataxia Telangiectasia, Ataxia Telangiectasia Mutated Proteins, Cell Cycle, Cell Cycle Proteins, DNA Damage, DNA-Binding Proteins, G2 Phase, Genes, p53, Humans, Models, Genetic, Phosphatidylinositol 3-Kinases, Phosphotransferases (Alcohol Group Acceptor), Protein-Serine-Threonine Kinases, Proteins, Tumor Suppressor Proteins