IndraLab

Statements



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"A similar result was obtained by treating neutrophils with extracellular KCl, which inhibits NLRP3 by blocking K + efflux (XREF_FIG and XREF_FIG)."

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"However, it was difficult to judge whether the effect of KCl was due to specific inhibition of the NLRP3 inflammasome, as the same concentration of KCl also decreased the cytokine responses of NLRP3 -/- macrophages to S. pneumoniae (data not shown)."

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"Extracellular KCl, which prevents K + efflux and NLRP3 dependent caspase-1 activation, abrogated UBE2L3 depletion (XREF_FIG D)."

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"High KCl is known to inhibit NLRP3 inflammasome activation and cell death by blocking K + efflux, a common trigger of NLRP3 inflammasome activation, as confirmed by the considerable reduction in released IL-1beta in the culture supernatant18, 19."

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"Notably, the association of NLRP3 with Nek7 as well as caspase-1 activation triggered by ATP were blocked in the presence of 50 mM KCl that inhibits potassium efflux and NLRP3 activation (XREF_FIG)."

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"The pretreatment of primary monocytes with MCC950, an NLRP3 inhibitor; YVAD, a caspase-1 inhibitor; or KCl, which prevents K efflux and inhibits activation of the canonical NLRP3 inflammasome [36], all resulted in a significant decrease in IL-1β release from infected primary human monocytes from multiple independent donors (Fig 1A)."