Cross-linking of SIGNR1 activates JNK and induces TNF-α production in RAW264.7 cells that express SIGNR1
Copyright policy )Cross-linking of SIGNR1 activates JNK and induces TNF-α production in RAW264.7 cells that express SIGNR1
In this study, we evaluated the signaling ability of SIGNR1 in murine macrophage-like RAW264.7 cells that stably expressed FLAG-tagged SIGNR1 (SIGNR1-FLAG). Cross-linking of SIGNR1-FLAG expressed on the cells by an anti-FLAG antibody induced JNK phosphorylation without induction of phosphorylation of ERK1/2 and p38 MAP kinase, and led to phosphorylations of Src family kinases (SFKs) and Akt. The SIGNR1-FLAG molecules in the cells were found in lipid raft-enriched membrane fractions, and the tyrosine kinases Lyn, Hck, and Fgr co-precipitated with SIGNR1-FLAG in the lipid raft fractions. The antibody-induced JNK phosphorylation was inhibited by inhibitors of SFKs and tyrosine kinases. Furthermore, cross-linking of SIGNR1 led to production of TNF-alpha, and the JNK inhibitor inhibited the antibody-induced TNF-alpha production. These results show that cross-linking of SIGNR1 triggers phosphorylation of SFKs, which leads to activation of the JNK pathway and induction of TNF-alpha production in macrophage-like RAW264.7 cells.
- Tokai University Japan
MAP Kinase Kinase 4, Tumor Necrosis Factor-alpha, Macrophages, Receptors, Cell Surface, Cell Line, Mice, Membrane Microdomains, src-Family Kinases, Animals, Lectins, C-Type, Phosphorylation, Cell Adhesion Molecules, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt
MAP Kinase Kinase 4, Tumor Necrosis Factor-alpha, Macrophages, Receptors, Cell Surface, Cell Line, Mice, Membrane Microdomains, src-Family Kinases, Animals, Lectins, C-Type, Phosphorylation, Cell Adhesion Molecules, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt
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