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. 2014 Jun 23;289(32):21973–21983. doi: 10.1074/jbc.M114.588723

FIGURE 1.

FIGURE 1.

Expression of CRADD and BCL10 in human and mouse endothelial cells and association of BCL10 with IRAK-1 in the proinflammatory TLR4 signaling pathway induced by LPS. CRADD mRNA and protein expression in endothelial cells was assessed by RT-PCR (A) and immunoblot analysis (B). C, BCL10 mRNA was assessed by RT-PCR in endothelial cells. In RT-PCR analyses, human negative control (HNC) and mouse negative control (MNC) reactions were performed using human or mouse primers, respectively, without cDNA. In immunoblot analyses, mouse spleen and liver extracts derived from cradd+/+ and cradd−/− mice served as positive (+/+) and negative (−/−) controls for CRADD protein, respectively, and β-actin served as a cellular protein loading control. D, co-immunoprecipitation of BCL10 with IRAK-1 is stimulus- and time-dependent. Primary cradd+/+ LMEC cells or human ST1.6 R endothelial cells were stimulated with 1 μg/ml of LPS for the indicated times. Protein complexes precipitated with anti-IRAK-1 (IP) from cell lysates were immunoblotted (IB) with antibodies to the indicated proteins. All gels and blots shown are representative of three independent experiments.