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. Author manuscript; available in PMC: 2008 Jul 1.
Published in final edited form as: Cell Signal. 2007 Apr 20;19(7):1372–1382. doi: 10.1016/j.cellsig.2007.03.013

Figure 3. Restraint of pro-inflammatory cytokine biosynthesis by MKP-1.

Figure 3

In response to microbial infection, TLRs initiate a series of signal transduction pathways, including NF-κB and MAP kinase cascades, leading to production of pro-inflammatory cytokines. Simultaneously, the signals initiated at the TLRs also induce MKP-1 gene transcription. ERK regulates MKP-1 expression by two mechanisms: by enhanceing MKP-1 gene transcription and by phosphorylating MKP-1 and thereby increasing its half-life. The MKP-1 protein in turn dephosphorylates JNK and p38, thus stopping the perpetuation of the inflammatory cascades and terminating cytokine production.