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The proinflammatory cytokine tumor necrosis factor-α (TNF-α) regulates immune responses, inflammation and programmed cell death. The ultimate fate of a cell exposed to TNF-αis determined by signal integration between its downstream effectors, including caspases, IKB kianse (IKK) and c-Jun N-terminal protein kinase (JNK). However, the molecular mechanisms are incompletely understood. We investigated this issue using genetic and biochemical approaches. We identified IKK β, a catalytic subunit of the IKK complex that is required for NF-KB activation and cell survival in response to TNF-α, was proteolyzed by casp-3-related caspases. This proteolysis eliminated IKK activity and promoted TNF-α, killing. Point
The ultimate fate of a cell exposed to TNF-αis determined by signal integration between its downstream effectors, including caspases, IKB kianse (IKK However, the molecular mechanisms are incompletely understood. We investigated this issue using genetic and biochemical approaches. We identified IKK β, a catalytic subunit of the IKK complex that is required for NF -KB activation and cell survival in response to TNF-α, was proteolyzed by casp-3-related caspases. This proteolysis eliminated IKK activity and promoted TNF-α, killing. Point