| First Author | Zeisel MB | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 11 | Pages | 7393-7 |
| PubMed ID | 15905587 | Mgi Jnum | J:98999 |
| Mgi Id | MGI:3580952 | Doi | 10.4049/jimmunol.174.11.7393 |
| Citation | Zeisel MB, et al. (2005) Cross talk between MyD88 and focal adhesion kinase pathways. J Immunol 174(11):7393-7 |
| abstractText | Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase involved in signaling downstream of integrins, linking bacterial detection, cell entry, and initiation of proinflammatory response through MAPKs and NF-kappaB activation. In this study, using protein I/II from Streptococcus mutans as a model activator of FAK, we investigated the potential link between FAK and TLR pathways. Using macrophages from TLR- or MyD88-deficient mice, we report that MyD88 plays a major role in FAK-dependent protein I/II-induced cytokine release. However, response to protein I/II stimulation was independent of TLR4, TLR2, and TLR6. The data suggest that there is a cross talk between FAK and MyD88 signaling pathways. Moreover, MyD88-dependent, LPS-induced IL-6 secretion by human and murine fibroblasts required the presence of FAK, confirming that MyD88 and FAK pathways are interlinked. |
