Can G. Pham

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During inflammation, NF-kappaB transcription factors antagonize apoptosis induced by tumor necrosis factor (TNF)alpha. This antiapoptotic activity of NF-kappaB involves suppressing the accumulation of reactive oxygen species (ROS) and controlling the activation of the c-Jun N-terminal kinase (JNK) cascade. However, the mechanism(s) by which NF-kappaB(More)
al., 2002). Cytotoxicity caused by ROS is mediated in part by the JNK pathway (Matsuzawa et al., 2002). Acti-During inflammation, NF-␬B transcription factors an-vation of this pathway by TNF␣ promotes death by in-tagonize apoptosis induced by tumor necrosis factor ducing cleavage of the Bcl-2 family BH3-only protein, (TNF)␣. This antiapoptotic activity of(More)
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