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Signal Pharmaceuticals other research news

April 12, 1999 7:00 AM UTC

Signal researchers and colleagues, along with separate groups at the University of California (San Diego, Calif.) and Hyogo College of Medicine (Hyogo, Japan) published in Science additional data on the mechanisms that activate the pro-inflammatory transcription factor NF-kB. Mice lacking IKKalpha, one subunit of an enzyme involved in NF-kB activation, had defects in limb, skeletal and skin morphogenesis but NF-kB from those mice was still activated in response to pro-inflammatory cytokines. Mice lacking IKKbeta, however, died as embryos due to liver damage from apoptosis. NF-kB in those mice was not activated by the tumor necrosis factor (TNF) cytokine, leading to the apoptosis in liver cells in response to TNF. ...