IndraLab

Statements

Calcium(2+) inhibits NLRP3. 21 / 21
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"Interestingly, Ca 2+ signaling contributes to dysregulated NLRP3 inflammasome activation in CAPS, a spectrum of autoinflammatory diseases caused by mutations in NLRP3 [XREF_BIBR]."
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"PS Inhibit ER Stress Induced Ca 2+ Accumulation, Which Then Downregulates the NLRP3 Inflammasome."
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"Lee et al. proposed a critical role for calcium sensing receptor (CASR) in activating the NLRP3 inflammasome that is mediated by increased intracellular Ca 2+ and decreased cellular cyclic AMP (cAMP) 21."
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"S1pr4 depletion in hepatic macrophages inhibited lipopolysaccharide-mediated Ca ++ release and deactivated the NLRP3 inflammasome."
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"These results suggest that TRPM2 knockdown reduces calcium level and inhibits NLRP3 activity under both physiological and pathological conditions."
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"Katsnelson et al. provided new insights that increasing LMP resulted in NLRP3 ubiquitination, and LMP induced Ca 2+ influx attenuated the association of NLRP3 with ASC [XREF_BIBR]."
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"The combination of increased cytosolic Ca 2+ and decreased cAMP was suggested to activate NLRP3."
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"Blockage of calcium mobilization by 2-APB, XeC, and U73122, the reduction of mitochondrial ROS by N-acetyl-L-cysteine and (2R,4R)-4-aminopyrro lidine-2,4-dicarboxylate, and the prevention of lysosomal rupture by a specific inhibitor to cathepsin, CA-074-Me, all inhibit NLRP3 inflammasome48)."
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"Nevertheless, there is currently no convincing explanation as to why in certain experimental systems the removal of extracellular Ca 2+ seems to inhibit NLRP3, while in other setups such treatment does not interfere with NLRP3 activation."
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"BAPTA, a strong Ca 2+ chelator and buffer of cytosolic Ca 2+, can inhibit NLRP3 inflammasome activation and IL-1beta processing independently of its function as a Ca 2+ chelator 28."
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"The absence of extracellular Ca 2+ effectively eliminated the increases in cytosolic [Ca 2+] in response to nigericin or ATP but did not attenuate NLRP3 inflammasome activation in BMDC."
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"The intracellular decrease of K + and increase of Ca 2+ levels trigger NLRP3 activation [XREF_BIBR]."
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"We tested the hypothesis that mDNA contributes to diabetes-associated endothelial dysfunction and vascular inflammation via NLRP3 activation.Methods: Vascular reactivity, reactive oxygen species (ROS) generation, calcium (Ca 2+ ) influx and caspase-1 and IL-1beta activation were determined in mesenteric resistance arteries from normoglicemic and streptozotocin-induced diabetic C57BL/6 and NLRP3 knockout (Nlrp3 -/- ) mice."
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"Activation of the NLRP3 inflammasome by ATP and other stimuli was reported to require Ca 2+ signaling as inhibition of Ca 2+ release from the ER and blocking extracellular Ca 2+ influx inhibited NLRP3 inflammasome function, presumably by preventing Ca 2+ induced mitochondrial damage."
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"Impaired Ca flux between ER and mitochondria also induces activation of the NLRP3 inflammasome (Missiroli et al., 2018)."
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"Methods : Vascular reactivity, reactive oxygen species (ROS) generation, calcium (Ca 2+) influx and caspase-1 and IL-1beta activation were determined in mesenteric resistance arteries from normoglicemic and streptozotocin induced diabetic C57BL/6 and NLRP3 knockout (Nlrp3 -/-) mice."
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"Because blocking TRPM2 mediated calcium mobilization drastically impaired caspase-1 activation and did not affect mitochondrial ROS production, it is possible that, unlike ER derived calcium, TRPM2 mediated calcium influx may directly signal activation of the NLRP3 inflammasome."
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"Recent studies suggest that nitric oxide (NO), Ca 2+ and cyclic AMP negatively regulate the NLRP3 inflammasome but the detailed mechanisms are unclear XREF_BIBR, XREF_BIBR."
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"The inhibition of intracellular calcium increase mediated by endoplasmic reticulum, store operated Ca 2+ entry and Ca 2+ entry from the extracellular milieu attenuate NLRP3 activation, and there is a consensus that intracellular Ca 2+ increase is associated to K + efflux [XREF_BIBR]."
33806797
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"Pretreatment or incubation in Ca -free medium with brief exposure to thapsigargin (Tg), a suppressant of the sarcoplasmic/ER Ca -ATPase (SERCA) pump, attenuates activation of the NLRP3 inflammasome."
34059091
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"Our results, for the first time, show that 3-HB-Gpr109a signaling promotes the influx of Ca 2+ under a normal physiological state and 3-HB-Gpr109a signaling mediated Ca 2+ influx represses NLRP3 inflammasome activation through PLC-IP3R pathway."
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