Critical role for calcium mobilization in activation of the NLRP3 inflammasome

By Tomohiko Murakami, Johan Ockinger, Jiujiu Yu, Vanessa Byles, A. McColl, A. Hofer, T. Horng. Proceedings of the National Academy of Sciences of the United States of America, 2012

880 citations recorded by the source corpus.

Subfields: Molecular Biology, Pediatrics, Perinatology and Child Health

View Paper: https://www.semanticscholar.org/paper/c393f4e9545610cc8af0fa99155eac628598955e

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In Molecular Biology

1. T. Kanneganti
2. G. Núñez
3. D. Sharma
4. S. Man
5. Yuan He
6. H. Hara
7. F. Sutterwala
8. Eric I. Elliott

Citations in the corpus

• Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation (2013, background): “Recent studies have implicated calcium flux and cAMP as critical regulators of Nlrp3 inflammasome activation (Lee et al., 2012; Murakami et al., 2012; Rossol et al., 2012; Zhong et al., 2013).”
• Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “Critically, Ca signaling and Ca flux alone is not sufficient for NLRP3 activation because only certain Gaq-coupled receptors and receptor tyrosine kinases (RTK) activate the inflammasome and the Ca ionophore ionomycin does not activate NLRP3 (71, 80).”
• An update on the regulatory mechanisms of NLRP3 inflammasome activation (2021, background): “Calcium signaling and calcium-sensing receptor (CaSR): Intracellular Ca flux plays an essential role in the assembly and activation of the NLRP3 inflammasome induced by multiple stimuli.(104,105) Studies showed that CaSR signaling promotes NLRP3 inflammasome assembly through intracellular Ca flux an”
• Redox Regulation of NLRP3 Inflammasomes: ROS as Trigger or Effector? (2015, neutral): “More recently, it was discovered that ATP induced Ca(2) + mobilization from both intracellular and extracellular stores, and that both inhibition of intracellular ER Ca(2) + stores by thapsigargin and incubation with Ca(2) + -free media to inhibit extracellular Ca(2) + entry were able to prevent ATP”
• The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “Production of reactive oxygen species (ROS), potassium efflux, changes in cell volume, calcium signaling, and lysosomal disruption have all been proposed as critical upstream signals required for NLRP3 activation (Cruz et al., 2007; Pétrilli et al., 2007; Cassel et al., 2008; Dostert et al., 2008; H”
• The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “Alternatively, it is proposed that the increase of cytosolic Ca2+ causes Ca2+ overloading of mitochondria, which induces mitochondrial dysfunction that leads to NLRP3 inflammasome activation [79].”
• Regulation of inflammasome activation (2015, background): “NLRs and ALRs mediate host recognition of pathogen-associated molecular patterns (PAMPs) released during bacterial, viral, fungal, and protozoan infections, or dangerassociated molecular patterns (DAMPs) released during cellular damage (1).”
• Mechanism and regulation of NLRP3 inflammasome activation (2016, background): “Alternatively, Ca mobilization and mitochondrial Ca overload may cause mitochondrial dysfunction, which may promote NLRP3 activation (see next subsection) [40].”