| First Author | De S | Year | 2015 |
| Journal | Proc Natl Acad Sci U S A | Volume | 112 |
| Issue | 31 | Pages | 9680-5 |
| PubMed ID | 26195767 | Mgi Jnum | J:226061 |
| Mgi Id | MGI:5695716 | Doi | 10.1073/pnas.1511794112 |
| Citation | De S, et al. (2015) Erlotinib protects against LPS-induced endotoxicity because TLR4 needs EGFR to signal. Proc Natl Acad Sci U S A 112(31):9680-5 |
| abstractText | Several components of the canonical pathway of response to lipopolysaccharide (LPS) are required for the EGF-dependent activation of NFkappaB. Conversely, the ability of Toll-like Receptor 4 (TLR4) to activate NFkappaB in response to LPS is impaired by down regulating EGF receptor (EGFR) expression or by using the EGFR inhibitor erlotinib. The LYN proto-oncogene (LYN) is required for signaling in both directions. LYN binds to the EGFR upon LPS stimulation, and erlotinib impairs this association. In mice, erlotinib blocks the LPS-induced expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) and ameliorates LPS-induced endotoxity, revealing that EGFR is essential for LPS-induced signaling in vivo. |
