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

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Lethality of Drosophila lacking TSC tumor suppressor function rescued by reducing dS6K signaling.

Tuberous sclerosis complex (TSC) is a genetic disorder caused by mutations in one of two tumor suppressor genes, TSC1 and TSC2. Here, we show that absence of Drosophila Tsc1/2 leads to constitutive dS6K activation and inhibition of dPKB, the latter effect being relieved by loss of dS6K. In contrast, the dPTEN tumor suppressor, a negative effector of PI3K, has little effect on dS6K, but negatively regulates dPKB. More importantly, we demonstrate that reducing dS6K signaling rescues early larval lethality associated with loss of dTsc1/2 function, arguing that the S6K pathway is a promising target for the treatment of TSC.[1]

References

  1. Lethality of Drosophila lacking TSC tumor suppressor function rescued by reducing dS6K signaling. Radimerski, T., Montagne, J., Hemmings-Mieszczak, M., Thomas, G. Genes Dev. (2002) [Pubmed]
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