The RLIG1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in the Jurkat T lymphocyte line, targeting the RLIG1 gene that encodes the RIG-I innate immune sensor. This cell pool provides a loss-of-function system for dissecting RNA-sensing pathways without clonal bias.
Jurkat cells, an immortalized human T cell line derived from acute T cell leukemia, are a standard model for T cell receptor signaling and leukemogenesis. Their intact innate signaling machinery makes them well-suited for exploring cytoplasmic nucleic acid recognition and antiviral pathways.
RLIG1 (RIG-I) operates as a cytosolic receptor for viral double-stranded and 5′-triphosphate RNA. Upon ligand binding and K63-linked ubiquitination by TRIM25, RIG-I engages the mitochondrial adaptor MAVS (IPS-1), triggering cascades via TRAF3/TRAF6, TBK1, and IKKepsilon kinases. This results in phosphorylation of IRF3 and IRF7, along with NF-kappaB activation, culminating in transcriptional induction of type I interferons (IFN-??/??) and ISGs. RIG-I function is modulated by cofactors including 14-3-3 epsilon, PACT, and ZAPS, and cross-regulates with LGP2 and MDA5 within the RLR network.
In Jurkat T cells, RLIG1 disruption eliminates RIG-I-dependent innate activation, offering a defined tool to study RNA sensing independently of other RLRs. This model is valuable for examining RIG-I signaling in the context of antiviral immunity, T cell-mediated inflammation, and cancer immunosurveillance, where RIG-I influences type I interferon responses and cellular apoptosis. The Jurkat background permits investigation of cross-regulation between RIG-I-MAVS and T cell receptor pathways.
Applications include quantification of IFN-?? and ISG induction by RT-qPCR and reporter assays following RNA stimulation, analysis of TBK1/IRF3 phosphorylation by western blot and flow cytometry, and co-immunoprecipitation of RIG-I complexes. The cells support viral infection assays (e.g., Sendai, influenza), RNA-seq transcriptomics, drug sensitivity testing with RIG-I agonists, and apoptosis profiling. This polyclonal knockout resource aids in dissecting RIG-I’s role in innate immunity and inflammation. For further assistance, contact Ascent Research.
