A schematic representation of how NLRP6 inhibits sepsis-induced microthrombosis formation. During systemic inflammation, pathogen-associated molecular patterns activate NLRP6, which leads to the polyubiquitination and subsequent degradation of the TAB1 protein. This degradation has 2 major downstream effects: (a) it inhibits the phosphorylation of key signaling proteins, including p65, IκBα, IKKβ, and TAK1, thereby impairing platelet function; and (b) it also inhibits the phosphorylation of SNAP23, preventing granule secretion. Together, the suppression of platelet activation and granule secretion disrupts microthrombosis formation during sepsis.

A schematic representation of how NLRP6 inhibits sepsis-induced microthrombosis formation. During systemic inflammation, pathogen-associated molecular patterns activate NLRP6, which leads to the polyubiquitination and subsequent degradation of the TAB1 protein. This degradation has 2 major downstream effects: (a) it inhibits the phosphorylation of key signaling proteins, including p65, IκBα, IKKβ, and TAK1, thereby impairing platelet function; and (b) it also inhibits the phosphorylation of SNAP23, preventing granule secretion. Together, the suppression of platelet activation and granule secretion disrupts microthrombosis formation during sepsis.

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