The human Toll signaling pathway: divergence of nuclear factor κB and JNK/SAPK activation upstream of tumor necrosis factor receptor–associated factor 6 (TRAF6)
The Journal of experimental medicine, 1998•rupress.org
The human homologue of Drosophila Toll (hToll) is a recently cloned receptor of the
interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of
adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of
the adapter molecule MyD88 and the IL-1R–associated kinase. Tumor necrosis factor
receptor–activated factor 6 (TRAF6) and the nuclear factor κB (NF-κB)–inducing kinase (NIK)
are both involved in subsequent steps of NF-κB activation. Conversely, a dominant negative …
interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of
adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of
the adapter molecule MyD88 and the IL-1R–associated kinase. Tumor necrosis factor
receptor–activated factor 6 (TRAF6) and the nuclear factor κB (NF-κB)–inducing kinase (NIK)
are both involved in subsequent steps of NF-κB activation. Conversely, a dominant negative …
The human homologue of Drosophila Toll (hToll) is a recently cloned receptor of the interleukin 1 receptor (IL-1R) superfamily, and has been implicated in the activation of adaptive immunity. Signaling by hToll is shown to occur through sequential recruitment of the adapter molecule MyD88 and the IL-1R–associated kinase. Tumor necrosis factor receptor–activated factor 6 (TRAF6) and the nuclear factor κB (NF-κB)–inducing kinase (NIK) are both involved in subsequent steps of NF-κB activation. Conversely, a dominant negative version of TRAF6 failed to block hToll-induced activation of stress-activated protein kinase/c-Jun NH2-terminal kinases, thus suggesting an early divergence of the two pathways.
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