Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome

By Takuma Misawa, Michihiro Takahama, Tatsuya Kozaki, Hanna Lee, J. Zou, T. Saitoh, Shizuo Akira. Nature Immunology, 2013

834 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/026aac0090b9f931905e6af9e1daf5c9abf5c6fd

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Citations in the corpus

• Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation (2013, background): “Consistent with other Nlrp3 agonists that have been demonstrated to induce mitochondrial dysfunction (Misawa et al., 2013; Zhou et al., 2011), we found that linezolid also induced mitochondrial”
• NLRP3 activation and mitosis are mutually exclusive events coordinated by NEK7, a new inflammasome component (2015, neutral): “Lys NLRP3 ASC WT K64M WT (1) Nek7 +/+ (GFP) (2) Nek7 (GFP) (3) Nek7 (GFP + NEK7) (4) Nek7 (GFP + NEK7(K64M))”
• Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome. (2016, background): “A possible mechanism for NLRP3 inflammasome activation is the accumulation of damaged, ROS-generating mitochondria (Misawa et al., 2013; Zhou et al., 2011).”
• The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “…colocalization of inflammasome components is required for all inflammasomes to be activated, inhibitors of microtubule alterations specifically block the NLRP3 inflammasome, suggesting that distinct cytoskeletal signatures are involved in activation of certain inflammasomes (Misawa et al., 2013).”
• An update on the regulatory mechanisms of NLRP3 inflammasome activation (2021, background): “3).(86,87) Indeed, the NLRP3 inflammasome complex can be assembled at highly specialized contact sites between the ER and mitochondria known as MAMs.”
• Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “Microtubule-dependent organelle transport was not driven by K efflux or mtROS, but instead involved increased a-tubulin acetylation by MEC-17 and decreased SIRT2-mediated deacetylation due to mitochondrial dysfunction and NAD depletion (37).”
• The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “It was also suggested that NLRP3 stimuli induce the transport of mitochondria to the ER, where the ASC present on the mitochondria come into close proximity to NLRP3 on the ER [109].”
• Colchicine --- update on mechanisms of action and therapeutic uses (2015, background): “The assembly of NALP3 in the endoplasmic reticulum with its adaptor, Apoptosis associated Speck like protein containing Caspase recruitment domain (ASC), is required for the activation of inflammasomes [21] [22][23].”
• Mitochondrial dysfunction in pathophysiology of heart failure (2018, background): “In addition to the release of mtDNA, recent studies suggest that mitochondrial redox state and NAD+ availability modulate NLRP3 activity (150, 151).”