IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling
The interleukin-1 receptor (IL-1R) signaling pathway leads to nuclear factor kappa B (NF-κB)
activation in mammals and is similar to the Toll pathway in Drosophila: the IL-1R–associated
kinase (IRAK) is homologous to Pelle. Two additional proximal mediators were identified
that are required for IL-1R–induced NF-κB activation: IRAK-2, a Pelle family member, and
MyD88, a death domain–containing adapter molecule. Both associate with the IL-1R
signaling complex. Dominant negative forms of either attenuate IL-1R–mediated NF-κB …
activation in mammals and is similar to the Toll pathway in Drosophila: the IL-1R–associated
kinase (IRAK) is homologous to Pelle. Two additional proximal mediators were identified
that are required for IL-1R–induced NF-κB activation: IRAK-2, a Pelle family member, and
MyD88, a death domain–containing adapter molecule. Both associate with the IL-1R
signaling complex. Dominant negative forms of either attenuate IL-1R–mediated NF-κB …
The interleukin-1 receptor (IL-1R) signaling pathway leads to nuclear factor kappa B (NF-κB) activation in mammals and is similar to the Toll pathway in Drosophila: the IL-1R–associated kinase (IRAK) is homologous to Pelle. Two additional proximal mediators were identified that are required for IL-1R–induced NF-κB activation: IRAK-2, a Pelle family member, and MyD88, a death domain–containing adapter molecule. Both associate with the IL-1R signaling complex. Dominant negative forms of either attenuate IL-1R–mediated NF-κB activation. Therefore, IRAK-2 and MyD88 may provide additional therapeutic targets for inhibiting IL-1–induced inflammation.
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