IndraLab

Statements


KCNMA1 activates NLRP3. 9 / 9
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"Like many other pore-forming toxins, SLO is TLR4 agonist and can induce proinflammatory cytokine expression (Park et al., 2004), and also activates the NLRP3 inflammasome to induce inflammatory cell death by pyroptosis of macrophages ( Figure 1 ) and the maturation and release of proinflammatory IL-1β (Timmer et al., 2009)."

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"Sublytic SLO Induces NLRP3 Inflammasome Activation and HMGB1 Release."

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"GAS expression of SLO may impair macrophage phagolysosomal fusion and acidification, facilitate GAS escape from the phagosome into the cytoplasm, block autophagic and xenophagic killing, or activate the NLRP3 inflammasome and IL-1beta production and pyroptosis."

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"In addition, and in contrast to several other Nlrp3 activating stimuli, these data also suggest that actin remodeling is not required for SLO mediated Nlrp3 inflammasome activation."

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"We tested whether sublytic SLO challenge promotes inflammasome activation by comparing Casp1 activation and HMGB1 secretion in WT, NLRP3 -/-, and Casp1 -/- BMDM treated with sublytic or lytic doses of SLO."

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"Additionally, the lack of the BK channel promoted the activation of the AIM2 inflammasome without affecting the activation of the NLRC4 and NLRP3 inflammasomes."

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"SLO also stimulates the activation of NLRP3 and caspase-1 in THP-1 macrophage-like cells (93)."

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"Nlrp3 inflammasome activation can be triggered by a number of stimuli, and although this inflammasome is the most extensively studied, the exact mechanism by which SLO, or any other stimulus, activates Nlrp3 is unclear."

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"We demonstrate that the lack of a BK channel specifically promoted AIM2 inflammasome activation without affecting NLRC4 and NLRP3 inflammasomes."