Molecular and Cellular Biology · 2012 · 42 citations · 51 references
Life SciencesImmunologyMolecular BiologyCell SignalingInflammationSignal TransductionCytokine BiologyCytokine SignalingCytokine-mediated PathologyInflammatory MediatorsInflammatory SignalingInnate Immune Signaling PathwaysC-jun N-terminal Kinase SignalingCaspase SignalingCaspase-4 ActivationCaspase-mediated Inflammatory SignalingImmunological MechanismsInflammatory Cytokine SecretionJun N-terminal Kinase SignalingNf-κb Signaling
Tumor necrosis factor alpha (TNF-α) is a potent inflammatory cytokine secreted upon cellular stress as well as immunological stimuli and is implicated in the pathology of inflammatory diseases and cancer. The therapeutic potential of modifying TNF-α pathway activity has been realized in several diseases, and antagonists of TNF-α have reached clinical applications. While much progress in the understanding of signaling downstream of the TNF-α receptor complex has been made, the compendium of factors required for signal transduction is still not complete. In order to find novel regulators of proinflammatory signaling induced by TNF-α, we conducted a genome-wide small interfering RNA screen in human cells. We identified several new candidate modulators of TNF-α signaling, which were confirmed in independent experiments. Specifically, we show that caspase 4 is required for the induction of NF-κB activity, while it appears to be dispensable for the activation of the Jun N-terminal protein kinase signaling branch. Taken together, our experiments identify caspase 4 as a novel regulator of TNF-α-induced NF-κB signaling that is required for the activation of IκB kinase. We further provide the genome-wide RNA interference data set as a compendium in a format compliant with minimum information about an interfering RNA experiment (MAIRE).
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Non-canonical inflammasome activation targets caspase-11
Nobuhiko Kayagaki, Søren Warming, Mohamed Lamkanfi et al. · Nature · 2011 · 2.5K citations