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

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ATM and the catalytic subunit of DNA-dependent protein kinase activate NF-kappaB through a common MEK/ extracellular signal-regulated kinase/p90(rsk) signaling pathway in response to distinct forms of DNA damage.

We have identified a novel pathway of ataxia telangiectasia mutated (ATM) and DNA-dependent protein kinase (DNA-PK) signaling that results in nuclear factor kappaB (NF-kappaB) activation and chemoresistance in response to DNA damage. We show that the anthracycline doxorubicin (DOX) and its congener N-benzyladriamycin (AD 288) selectively activate ATM and DNA-PK, respectively. Both ATM and DNA-PK promote sequential activation of the mitogen-activated protein kinase (MAPK)/p90(rsk) signaling cascade in a p53-independent fashion. In turn, p90(rsk) interacts with the IkappaB kinase 2 ( IKK-2) catalytic subunit of IKK, thereby inducing NF-kappaB activity and cell survival. Collectively, our findings suggest that distinct members of the phosphatidylinositol kinase family activate a common prosurvival MAPK/IKK/NF-kappaB pathway that opposes the apoptotic response following DNA damage.[1]

References

  1. ATM and the catalytic subunit of DNA-dependent protein kinase activate NF-kappaB through a common MEK/extracellular signal-regulated kinase/p90(rsk) signaling pathway in response to distinct forms of DNA damage. Panta, G.R., Kaur, S., Cavin, L.G., Cortés, M.L., Mercurio, F., Lothstein, L., Sweatman, T.W., Israel, M., Arsura, M. Mol. Cell. Biol. (2004) [Pubmed]
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