Temporal Control of TNFα Signaling by Miz1
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.
- 3.Liu J, Zhao Y, Eilers M, Lin A (2009) Miz1 is a signal- and pathway-specific modulator or regulator (SMOR) that suppresses TNFα-induced JNK activation. PNAS Oct 7. [Epub ahead of print]Google Scholar