Inflammasome Test Cells
The role of ASC in canonical inflammasomes
Inflammasomes are key signaling platforms that typically comprise a sensor, the ASC adaptor, and pro-caspase-1. To date, there have been five receptor proteins or 'sensors' confirmed to assemble 'canonical' inflammasomes, and these include NLRP1, NLRP3, and NLRC4, as well as the proteins, absent in melanoma 2 (AIM2) and pyrin [1]. These canonical inflammasomes are complemented by the non-canonical pathway, which involves caspase 11 (CASP11) in mice and its human orthologs caspase 4 (CASP4) and caspase 5 (CASP5) [2]. Inflammasomes will assemble in response to a diverse range of pathogen-associated or danger-associated molecular patterns (PAMPs or DAMPs) such as outer membrane vesicles (OMVs) and sterile stressors (i.e. K+ efflux), respectively. Ultimately, activation of inflammasomes leads to the cleavage and activation of caspase-1, which induces the maturation and secretion of the highly pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18. Additionally, activated CASP1, as well as the non-canonical inflammasomes, CASP11-4/5, cleave the pore-forming protein gasdermin D (GSDMD), which leads to a form of inflammatory cell death termed pyroptosis.
To foster inflammasome research, InvivoGen provides a growing collection of cell lines derived from either the human monocytic THP1 cell line, which is widely used for inflammasome studies due to its high expression levels of NLRP3, ASC, and pro-caspase-1, or the murine macrophage RAW 264.7 cell line.
The collection is comprised of:
- KO/KD/OE cells: Inflammasome gene of interest has been knockout (KO), knockdown/deficient (KD) or overexpressed (OE)
- Reporter cells: For the monitoring of inflammasome activity
- Parental cells: Positive controls for KO/KD inflammasome studies
Download our Practical guide on Inflammasomes
References:
1. Broz, P. & Dixit, V.M. 2016. Inflammasomes: mechanism of assembly, regulation, and signaling. Nat Rev Immunol 16, 407-420.
2. Russo, A.J. et al. 2018. Emerging Insights into Noncanonical Inflammasome Recognition of Microbes. J Mol Biol 430, 207-216.