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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Lack of PTEN sequesters CHK1 and initiates genetic instability.

Pten-/- cells display a partially defective checkpoint in response to ionizing radiation (IR). The checkpoint defect was traced to the ability of AKT to phosphorylate CHK1 at serine 280, since a nonphosphorylated mutant of CHK1 (S280A) complemented the checkpoint defect and restored CDC25A degradation. CHK1 phosphorylation at serine 280 led to covalent binding of 1 to 2 molecules of ubiquitin and cytoplasmic CHK1 localization. Primary breast carcinomas lacking PTEN expression and having elevated AKT phosphorylation had increased cytoplasmic CHK1 and displayed aneuploidy (p <0.005). We conclude that loss of PTEN and subsequent activation of AKT impair CHK1 through phosphorylation, ubiquitination, and reduced nuclear localization to promote genomic instability in tumor cells.[1]

References

  1. Lack of PTEN sequesters CHK1 and initiates genetic instability. Puc, J., Keniry, M., Li, H.S., Pandita, T.K., Choudhury, A.D., Memeo, L., Mansukhani, M., Murty, V.V., Gaciong, Z., Meek, S.E., Piwnica-Worms, H., Hibshoosh, H., Parsons, R. Cancer Cell (2005) [Pubmed]
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