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Previously, we found that endogenously produced pro‐inflammatory molecules, advanced glycation end products (AGEs), interact with tumor necrosis factor‐like weak inducer of apoptosis (TWEAK), and attenuate its immunomodulatory function. In the present study, to elucidate the mechanism by which AGEs attenuate TWEAK function, we searched for regions responsible for TWEAK–AGE interaction using TWEAK...
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