The IRGQ Knockout PaTu 8988t Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the IRGQ gene has been disrupted using a non-homologous end joining-based knockout strategy. This polyclonal pool contains a heterogeneous mixture of edited alleles, enabling the study of IRGQ loss-of-function in a cellular context that closely models metastatic pancreatic cancer. Unlike monoclonal cell lines, the polyclonal format preserves population-level diversity and is particularly suited for assays where clonal variation is not desired, such as bulk proteomics, pooled functional screens, and population-based phenotypic analyses. The product is supplied as a ready-to-use cryopreserved stock of early-passage cells, each lot verified for target gene disruption by Sanger sequencing and immunoblotting before release.
PaTu 8988t is a human pancreatic ductal adenocarcinoma cell line originally established from a liver metastasis. This cell line retains key molecular features of aggressive pancreatic cancer, including mutations in KRAS and TP53, high metastatic potential, and a secretory phenotype that shapes the tumor microenvironment. PaTu 8988t cells grow as an adherent monolayer in standard culture conditions and are widely used to model the biology of metastatic dissemination, chemoresistance, and tumor?Cstroma interactions. Their hepatic origin makes them especially relevant for investigating organ-specific tropism and immune evasion mechanisms that allow pancreatic cancer cells to colonize distant sites.
IRGQ encodes an interferon-inducible GTPase that plays a critical role in cell-autonomous immunity by mediating the autophagic restriction of Toxoplasma gondii. Upon stimulation by interferon-gamma (IFN-??) via JAK-STAT signaling, IRGQ is recruited to the parasitophorous vacuole membrane, where it directly interacts with the SNARE protein STX17. This interaction tethers autophagosomes to the vacuole, and together with ATG5 and the ubiquitin-like protein GABARAPL2, promotes LC3 lipidation and lysosomal fusion, ultimately leading to vacuole acidification and parasite killing. Beyond anti-parasitic defense, IRGQ participates more broadly in autophagy-related membrane trafficking and innate immune responses, forming complexes with ATG5, GABARAPL2, and LC3/GABARAP family members to facilitate xenophagy.
In the context of PaTu 8988t cells, disrupting IRGQ provides a powerful tool to dissect the intersection of autophagy and immune signaling in pancreatic cancer metastasis. Because PaTu 8988t cells originated from a liver metastasis, they are likely adapted to survive innate immune pressures, and IRGQ may contribute to immune evasion by modulating autophagic flux or interferon responses. The knockout model enables investigation of whether IRGQ deficiency alters the susceptibility of pancreatic cancer cells to immune-mediated clearance, changes their metastatic capacity, or reprograms the autophagy-lysosome pathway. Additionally, these cells can serve as a negative control for experiments involving Toxoplasma infection or other intracellular pathogens, as IRGQ is essential for IFN-??-dependent restriction.
Typical research applications include innate immunity and host-pathogen studies, where researchers can assess Toxoplasma gondii replication by flow cytometry or immunofluorescence and measure IFN-??-inducible gene expression by RT-qPCR. Autophagy mechanisms can be interrogated by western blotting for IRGQ, LC3 lipidation, and ATG5, as well as by co-immunoprecipitation of IRGQ-STX17 complexes. In cancer biology, the knockout cells are useful for evaluating the role of IRGQ in metastatic behavior, immune microenvironment modulation, and response to autophagy-modulating therapeutics. All experimental designs should include appropriate parental cell controls and consider the polyclonal nature of the population when interpreting functional outcomes. For detailed product specifications, lot-specific validation data, or technical support, please contact Ascent Research.
