Abstract
The pro-inflammatory cytokine tumor necrosis factor (TNFα) regulates a wide range of biological activities, including inflammation, immune responses, apoptosis, and tumorigenesis mainly through its cytoplasm membrane receptor TNF-R1 complex 1 [6,7], which activates downstream effectors such as NF-κB, caspases and JNK. However, the control of TNF-R1 complex 1 activity is incompletely understood. We report here that the transcription factor zinc finger protein Mizl selectively inhibits TNFα-induced JNK activation in a transcription-independent manner and has to be removed upon TNFα stimulation. Our results suggest a de-repression model for TNFα-induced JNK activation.
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Lin, A. (2011). Temporal Control of TNFα Signaling by Miz1. In: Wallach, D., Kovalenko, A., Feldmann, M. (eds) Advances in TNF Family Research. Advances in Experimental Medicine and Biology, vol 691. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-6612-4_13
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DOI: https://doi.org/10.1007/978-1-4419-6612-4_13
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