A Protective Role for the Human SMG-1 Kinase against Tumor Necrosis Factor-alpha induced Apoptosis

Oliveira, V., Romanow, W.J., Geisen, C., Otterness, D.M., Mercurio, F., Wang, H.G., Dalton, W.S., Abraham, R.T.
Journal   J Biol Chem.
Species  
Analytes Measured   Caspase-3
Matrix Tested   U2OS osteosarcoma cell lysates
Year   2008
Volume   283
Page Numbers   13174-13184
Application   Phosphoproteins
Abstract
The human suppressor of morphogenesis in genitalia-1 (hSMG-1) protein kinase plays dual roles in mRNA surveillance and genotoxic stress response pathways in human cells. Here, we report that small interfering RNA-mediated depletion of hSMG-1, but not ATM, ATR, hUpf1, or hUpf2, in human U2OS osteosarcoma cells markedly increases the magnitude and accelerates the rate of apoptosis induced by tumor necrosis factor-alpha (TNFalpha) stimulation. The increase in TNFalpha-mediated cell killing observed in hSMG-1-depleted cells is not related to the suppression of nonsense-mediated mRNA decay or to the inhibition of TNFalpha-induced NF-kappaB activation. Rather, we observed that loss of hSMG-1 accelerates the degradation of the long form of the FLICE-inhibitory protein (FLIP(L)), an inhibitor of death-inducing signaling complex-mediated caspase-8 activation, in TNFalpha-treated cells. These results suggest that hSMG-1 plays an important role in cell survival during TNFalpha-induced stress.

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