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. Author manuscript; available in PMC: 2014 Dec 28.
Published in final edited form as: J Immunol. 2011 Jan 28;186(5):3180–3187. doi: 10.4049/jimmunol.1001252

FIGURE 7.

FIGURE 7

p120 suppresses TLR4 signaling. RLMVECs grown to 50– 70% confluence were transfected with scrambled (Sc) and p120 siRNA. At 48 h posttransfection, cells were exposed to LPS (1.0 μg/ml) for the indicated times. A, Effect of p120 knockdown on the interaction of TLR4 and MyD88. Immunoprecipitation of TLR4 and immunoblotting with Ab against MyD88 were performed. The association of MyD88 and TLR4 was augmented in p120 knockdown endothelial cells. B, Effect of over-expression of p120 on the interaction of TLR4 and MyD88. Over-expression of p120 was performed by transfecting RLMVECs with LZRS retrovirus containing murine p120 1A cDNA or control vector. At 72 h posttransfection, cells were exposed to LPS (1.0 μg/ml) for the indicated times. C, Effect of p120 expression on IRAK-4 kinase activity in lung endothelial cells following LPS stimulation. RLMVECs were challenged with LPS for the indicated times and immunoprecipitation of IRAK-4 was performed. IRAK-4 kinase activity was measured by γ[32P] incorporation of MBP used as substrate (see Materials and Methods for details). Data are representative of three independent experiments.