IndraLab

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"As shown in Fig. 4, either H2O2- or V2O5 induced STAT-1 activation was blocked by pretreatment of cells with the EGFR tyrosine kinase inhibitor AG1478."
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"V2O5 induced STAT-1 activation was blocked by catalase and N-acetyl-L-cysteine (NAC), suggesting vanadiuminduced generation of H2O2."
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"However, it remains unclear whether vanadium activates STAT-1 via the generation of H2O2, other ROS, or through an oxidant independent mechanism.In the present study, we found that V2O5 induced STAT-1 activation was significantly inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and the H2O2scavenger catalase, indicating that H2O2 was required for V2O5 induced STAT-1 activation."
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"However, we observed that V2O5 induced STAT-1 activation was not inhibited by neutralizing antibodies raised against IFN-␥, IFN-␤, or IFN- (unpublished observation)."
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