CASP4 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal human T lymphoblast population with targeted disruption of the CASP4 gene. This loss-of-function model enables investigation of non-canonical inflammasome signaling and pyroptosis in a Jurkat background. The polyclonal mixture of edited alleles provides robust population-level analysis while avoiding clonal artifacts. CRISPR/Cas9-mediated gene disruption abrogates functional caspase-4 expression, offering a clean system to dissect CASP4-dependent pathways.
The Jurkat cell line is derived from a 14-year-old male with acute T cell leukemia and serves as a widely used suspension model for T lymphocyte signaling and apoptosis studies. Its lymphoblastic origin and sensitivity to death stimuli make it ideal for examining programmed cell death mechanisms. This CASP4 knockout in Jurkat cells allows direct interrogation of inflammatory caspase function in a T cell context, relevant to immune regulation and hematological malignancies.
CASP4 encodes an inflammatory caspase acting as an intracellular LPS receptor. Upon LPS binding, it oligomerizes and autoactivates, triggering non-canonical inflammasome activation. Active CASP4 cleaves gasdermin D (GSDMD) to generate membrane pores, leading to pyroptosis and release of IL-1?? and HMGB1. Upstream regulators include TLR4, type I interferons, and IRF3. CASP4 also interacts with CASP5 and NLRP3 inflammasome components, and is linked to ER stress-induced apoptosis.
In Jurkat T lymphoblasts, this knockout model dissects non-canonical inflammasome contributions to pyroptosis without confounding canonical inflammasome activity, as Jurkat cells lack certain canonical components. It enables clean study of CASP4-mediated intracellular LPS responses downstream of TLR4 and type I interferon signaling. Moreover, the system facilitates exploration of ER stress crosstalk with inflammatory caspase activation and the role of pyroptosis in T cell homeostasis and leukemia.
This product is suited for mechanistic inflammasome studies, inhibitor screening, and disease modeling in septic shock or inflammatory bowel disease. Compatible assays include Western blotting for CASP4 and GSDMD cleavage, LDH release, IL-1?? ELISA, flow cytometry, qPCR, co-immunoprecipitation with LPS, and pyroptotic morphology microscopy. For additional details, please contact Ascent Research.
