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Cutting Edge: Monarch-1 Suppresses Non-Canonical NF-{kappa}B Activation and p52-Dependent Chemokine Expression in Monocytes.

CATERPILLER (NOD, NBD-LRR) proteins are rapidly emerging as important mediators of innate and adaptive immunity. Among these, Monarch-1 operates as a novel attenuating factor of inflammation by suppressing inflammatory responses in activated monocytes. However, the molecular mechanisms by which Monarch-1 performs this important function are not well understood. In this report, we show that Monarch-1 inhibits CD40-mediated activation of NF-kappaB via the non-canonical pathway in human monocytes. This inhibition stems from the ability of Monarch-1 to associate with and induce proteasome-mediated degradation of NF-kappaB inducing kinase. Congruently, silencing Monarch-1 with shRNA enhances the expression of p52-dependent chemokines.[1]

References

  1. Cutting Edge: Monarch-1 Suppresses Non-Canonical NF-{kappa}B Activation and p52-Dependent Chemokine Expression in Monocytes. Lich, J.D., Williams, K.L., Moore, C.B., Arthur, J.C., Davis, B.K., Taxman, D.J., Ting, J.P. J. Immunol. (2007) [Pubmed]
 
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