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Temporal Control of TNFα Signaling by Miz1

  • Anning Lin
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 691)

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.

Keywords

Death Domain Protein Transcription Factor Zinc Finger Protein Factor Zinc Finger Factor Zinc Kinase SAPK 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Cryns V, Yuan J (1998) Proteases to die for. Genes Dev 12:1551–1570CrossRefPubMedGoogle Scholar
  2. 2.
    Hsu H, Shu HB, Pan MG, Goeddel DV (1996) TRADD-TRAF2 and TRADD FADD interactions define two distinct TNF receptor 1 signal transduction pathways. Cell 84:299–308CrossRefPubMedGoogle Scholar
  3. 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
  4. 4.
    Micheau O, Tschopp J (2003) Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes. Cell 114:181–190CrossRefPubMedGoogle Scholar
  5. 5.
    Muzio M, Chinnaiyan AM, Kischkel FC, O’Rourke K, Shevchenko A, Ni J, Scaffidi C, Bretz JD, Zhang M, Gentz R et al (1996) FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death—inducing signaling complex. Cell 85:817–827CrossRefPubMedGoogle Scholar
  6. 6.
    Tartaglia LA, Goeddel DV (1992). Two TNF receptors. Immunol Today 13:151–153CrossRefPubMedGoogle Scholar
  7. 7.
    Tracey KJ, Cerami A (1994) Tumor necrosis factor: a pleiotropic cytokine and therapeutic target. Annu Rev Med 45:491–503CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Ben May Department for Cancer ResearchUniversity of ChicagoChicagoUSA

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