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TNF-induced MAP kinase activation oscillates in time.

Jameel Iqbal1, Mone Zaidi

  • 1Department of Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, P.O. Box 1055, New York, NY 10029, USA.

Biochemical and Biophysical Research Communications
|April 4, 2008
PubMed
Summary

Tumor necrosis factor (TNF) triggers dynamic oscillations in multiple signaling pathways, not just mRNA production. These cyclical activations, involving MAP kinases and p65, reveal a new paradigm in cellular signaling.

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Area of Science:

  • Cellular signaling and systems biology
  • Molecular and cellular biology
  • Immunology

Background:

  • Tumor necrosis factor (TNF) signaling is crucial for cellular responses.
  • Previous studies identified oscillations in mRNA production downstream of TNF.
  • Limited understanding of oscillatory dynamics in TNF-induced signaling pathways.

Purpose of the Study:

  • To investigate oscillations in signaling components downstream of the TNF receptor.
  • To determine if multiple signaling pathways exhibit cyclical activation upon TNF stimulation.
  • To elucidate the role of NF-kappaB in TNF-induced signaling oscillations.

Main Methods:

  • Analysis of time-series microarray data from TNF-treated cells.
  • Western blotting to detect phosphorylation of signaling molecules.
  • Utilizing an NF-kappaB super-repressor to assess its impact on oscillations.

Main Results:

  • TNF stimulation induces oscillations in multiple signaling components beyond mRNA, including TRAF1.
  • Phosphorylation of three MAP kinases and p65 exhibit oscillatory patterns.
  • An NF-kappaB super-repressor modulates but does not abolish MAPK phosphorylation oscillations.

Conclusions:

  • TNF signaling involves widespread oscillatory activation of downstream pathways.
  • NF-kappaB acts as a modulator, not the sole driver, of these cyclical signaling events.
  • Dynamic, time-resolved measurements are essential for understanding kinase phosphorylation in cellular signaling.