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Structural basis of human IL-18 sequestration by the decoy receptor IL-18 binding protein in inflammation and tumor immunity
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TRAIL receptors serve as stress-associated molecular patterns to promote ER-stress-induced inflammation
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To NET or not to NET : current opinions and state of the science regarding the formation of neutrophil extracellular traps
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Suppressing IL-36-driven inflammation using peptide pseudosubstrates for neutrophil proteases
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- Journal Article
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Mind bomb regulates cell death during TNF signaling by suppressing RIPK1's cytotoxic potential
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iTAP, a novel iRhom interactor, controls TNF secretion by policing the stability of iRhom/TACE
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Identification of small-molecule elastase inhibitors as antagonists of IL-36 cytokine activation
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Extracellular neutrophil proteases are efficient regulators of IL-1, IL-33, and IL-36 cytokine activity but poor effectors of microbial killing
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Neutrophil extracellular traps can serve as platforms for processing and activation of IL-1 family cytokines
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Production of biologically active IL-36 family cytokines through insertion of N-terminal caspase cleavage motifs
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Getting a gRIP on flu by casting the DAI
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Neutrophil-derived proteases escalate inflammation through activation of IL-36 family cytokines
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Necroptosis suppresses inflammation via termination of TNF- or LPS-induced cytokine and chemokine production
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Diverse activators of the NLRP3 inflammasome promote IL-1 beta secretion by triggering necrosis
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RIPK1 can function as an inhibitor rather than an initiator of RIPK3-dependent necroptosis