IRGQ Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the IRGQ gene in the Jurkat T lymphoblast cell line. This gene-edited pool offers a loss-of-function model to investigate the functional roles of the immunity-related GTPase IRGQ in T-cell biology, notably in autophagy and innate immune signaling pathways.
The Jurkat cell line, derived from the peripheral blood of a 14-year-old male with acute T cell leukemia, is a widely used model for T lymphocyte signaling and apoptosis. These suspension cells express surface markers CD3, CD4, and the interleukin-2 receptor, enabling studies on T-cell receptor?Cmediated activation, signal transduction, and programmed cell death.
IRGQ encodes an immunity-related GTPase that predominantly localizes to the Golgi apparatus and autophagosomes. Mechanistically, IRGQ binds to the ATG5-ATG12 conjugate and recruits it to membranes, where it facilitates the lipidation of LC3/GABARAP family proteins and promotes autophagosome elongation. This activity is critical for the engulfment and lysosomal degradation of cytosolic pathogens. Upstream, IRGQ expression is induced by interferon-gamma (IFN-??), type I interferons, and toll-like receptor stimulation, while mTORC1 inhibition and nutrient deprivation further activate the protein. Downstream, IRGQ drives autophagosome formation and stabilizes the ATG5-ATG12 complex. In addition to the core ATG factors, IRGQ interacts with WIPI2, Beclin1, PIK3C3/VPS34, and RAB GTPases, linking it to the ULK1 complex and PI3K-III complex that govern autophagy initiation and maturation.
In Jurkat T lymphoblasts, IRGQ knockout provides a unique tool to dissect the intersection between autophagy and T-cell function. Given the central roles of autophagy in lymphocyte homeostasis, antigen presentation, and survival, this polyclonal knockout pool allows researchers to examine how loss of IRGQ affects T-cell activation, proliferation, or apoptosis without clonal bias. It is particularly valuable for interrogating the dependency of acute T cell leukemia cells on autophagic processes, as well as for identifying synthetic lethal interactions or resistance mechanisms to autophagy-modulating agents.
Typical applications include investigating autophagy regulation in T lymphocytes via LC3 puncta immunofluorescence or LC3-II turnover analysis by western blot, studying host defense using intracellular pathogen clearance assays, and assessing cell viability under nutrient-deprived conditions. The cells also enable co-immunoprecipitation studies to probe IRGQ-ATG5 interaction and GTPase activity measurements. Furthermore, flow cytometry?Cbased autophagic flux assays can quantify the impact of IRGQ disruption on degradative output. For detailed information or to inquire about bulk orders, please contact Ascent Research.
