Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf

By S. Mariathasan, K. Newton, D. Monack, D. Vučić, D. French, Wyne P. Lee, Merone Roose-Girma, S. Erickson, V. Dixit. Nature, 2004

1,905 citations recorded by the source corpus.

Subfields: Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/9f409bfbcf8648d2987bfd0b15c67095ee3e6f1e

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In Molecular Biology

1. J. Tschopp
2. T. Kanneganti
3. G. Núñez
4. M. Lamkanfi
5. Kate Schroder
6. V. Dixit
7. Shizuo Akira
8. S. Man

In Surgery

1. J. Tschopp
2. T. Kanneganti
3. Kate Schroder
4. S. Man
5. M. Lamkanfi
6. H. Hammad
7. B. Lambrecht
8. Shizuo Akira

Citations in the corpus

• Regulation of inflammasome signaling (2012, background): “Although ASC is not an absolute requirement, it substantially augments NLRC4-mediated inflammasome activatio”
• Regulation of inflammasome activation (2015, background): “This interaction may explain why NLRC4 is able to induce pyroptosis independently of ASC (13, 150).”
• The pyroptosome: a supramolecular assembly of ASC dimers mediating inflammatory cell death via caspase-1 activation (2007, background): “Preliminary studies showed that IPAF forms an inflammasome complex with caspase-1 in response to infection of mouse macrophages with Salmonella.(19) Interestingly, although ASCdeficient mouse macrophages contain IPAF, they showed delayed cell death and no detectable caspase-1 activation in response ”
• A Proposed Classification of the Immunological Diseases (2006, background): “It now appears that TRAPS and other monogenic periodic fever disorders share a common thread. They all show disturbances in pathways associated with innate immune cell function, encompassing abnormal signalling in key cytokine pathways that include TNF and interleukin-1 (IL-1s) (via adaptor molecule”
• Role of pyroptosis in inflammation and cancer (2022, background): “Nevertheless, the presence of ASC can substantially augment NLRC4-mediated pyroptosis [55, 56].”
• The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “NLRC4 activates procaspase-1 through its CARD domain to induce cell death (Poyet et al., 2001) in response to Salmonella infection (Mariathasan et al., 2004).”
• Deubiquitination of NLRP3 by BRCC3 critically regulates inflammasome activity. (2013, background): “Typhimurium or cytosolic poly(dA-dT) DNA, which are dependent on the NLRC4 and AIM2 inflammasomes, respectively, and independent of NLRP3 (Figures S2A–S2F) (Fernandes-Alnemri et al., 2009; Mariathasan et al., 2004).”
• Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome (2009, background): “In contrast, M deficient in Nlrc4, which is required for caspase-1 activation in response to infection with type III and type IV secretion system carrying Gram-negative bacteria (15, 16), were capable of secreting IL-1 in response to complement-lysed splenocytes (Fig.”
• Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin (2006, background): “Furthermore, mouse macrophages that lack Ipaf or ASC are resistant to lysis by Salmonella typhimurium”
• GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death (2016, positive): “Infection of primary murine bone marrow-derived macrophages (BMDMs) with Salmonella enterica serovar Typhimurium ( S. typhimurium ) activates the NLRC4 inflammasome (Mariathasan et al , 2004) and results in caspase-1-and GSDMD-dependent pyrop-tosis and cytokine release (Appendix Fig S1C and D).”