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- W2051200214 abstract "Damage to the mitotic spindle and centrosome dysfunction can lead to cancer. To prevent this, cells trigger a succession of checkpoint responses, where an initial mitotic delay is followed by slippage without cytokinesis, spawning tetraploid G1 cells that undergo a p53-dependent G1/S arrest. We describe the importance of Lats2 (Large Tumor Suppressor 2) in this checkpoint response. Lats2 binds Mdm2, inhibits its E3 ligase activity, and activates p53. Nocodazole, a microtubule poison that provokes centrosome/mitotic apparatus dysfunction, induces Lats2 translocation from centrosomes to the nucleus and p53 accumulation. In turn, p53 rapidly and selectively up-regulates Lats2 expression in G2/M cells, thereby defining a positive feedback loop. Abrogation of Lats2 promotes accumulation of polyploid cells upon exposure to nocodazole, which can be prevented by direct activation of p53. The Lats2-Mdm2-p53 axis thus constitutes a novel checkpoint pathway critical for the maintenance of proper chromosome number." @default.
- W2051200214 created "2016-06-24" @default.
- W2051200214 creator A5003965483 @default.
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- W2051200214 date "2006-10-01" @default.
- W2051200214 modified "2023-10-16" @default.
- W2051200214 title "A positive feedback loop between the p53 and Lats2 tumor suppressors prevents tetraploidization" @default.
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- W2051200214 doi "https://doi.org/10.1101/gad.1447006" @default.
- W2051200214 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1578695" @default.
- W2051200214 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17015431" @default.
- W2051200214 hasPublicationYear "2006" @default.
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