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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Diverse Toll-like receptors utilize Tpl2 to activate extracellular signal-regulated kinase ( ERK) in hemopoietic cells.

Engaging mammalian Toll-like receptors (TLRs) activate both the NF-kappaB and mitogen-activated protein kinase signaling pathways. Here we establish that mitogen-activated protein 3 kinase Tpl2, levels of which are markedly reduced in nfkb1(-/-) cells, is required for extracellular signal-regulated kinase ( ERK) activation in bone marrow-derived macrophages and B cells stimulated with diverse TLR ligands. Despite rescuing TLR-dependent ERK activation in nfkb1(-/-) bone marrow-derived macrophages by using an estrogen receptor-regulated version of the mitogen-activated protein 3 kinase, c-Raf (Raf:ER), CpG or LPS induction of IL-10 was only partially restored in nfkb1(-/-) cells expressing Raf:ER, a finding consistent with NF-kappaB1 regulating IL-10 by a combination of ERK-independent and -dependent mechanisms. Collectively, our findings indicate that the Tpl2/MEK/ ERK signaling module is a master regulator of ERK-dependent gene expression downstream of TLRs in different hemopoietic cells.[1]

References

  1. Diverse Toll-like receptors utilize Tpl2 to activate extracellular signal-regulated kinase (ERK) in hemopoietic cells. Banerjee, A., Gugasyan, R., McMahon, M., Gerondakis, S. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
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