The IRGQ Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in which the human IRGQ gene has been disrupted via targeted genome editing. This loss-of-function model enables the study of IRGQ within its native genomic context in the 143B host cell line, providing a robust tool for autophagy and innate immunity investigations. The polyclonal format represents a heterogeneous pool of edited cells, allowing analysis of diverse knockout outcomes without clonal artifacts.
Derived from a human osteosarcoma, the 143B cell line is a widely used model in bone cancer research. It retains aggressive tumorigenic and metastatic properties characteristic of osteosarcoma, making it suitable for studies on tumor biology, metastasis, and drug resistance. The stable genetic background of 143B ensures reliable generation and propagation of gene-edited derivatives.
IRGQ, a member of the immunity-related GTPase family, is an interferon-inducible GTPase pivotal for autophagy-mediated innate defense. It is transcriptionally regulated by IFN-?? and type I interferons via JAK/STAT signaling. Following induction, IRGQ localizes to autophagic membranes and interacts with ATG proteins and the adaptor SQSTM1/p62 to drive autophagosome maturation. Downstream, IRGQ promotes LC3 lipidation and Beclin-1 recruitment, facilitating lysosomal degradation of intracellular pathogens. Through these interactions, IRGQ couples interferon signaling to the autophagy machinery.
In the 143B osteosarcoma background, IRGQ knockout disrupts autophagy regulation and innate immune pathways, potentially impacting tumor cell survival, migration, and drug sensitivity. Because osteosarcoma cells depend on autophagy for metabolic adaptation and stress resistance, this model enables dissection of interferon-driven autophagy in bone cancer biology and immune evasion mechanisms.
These polyclonal knockout cells support diverse assays: western blotting for LC3-II, RT-qPCR for gene expression, immunofluorescence for LC3 or WIPI2, and flow cytometry for viability and apoptosis. Migration, invasion, and drug sensitivity assays further facilitate osteosarcoma metastasis and therapeutic studies. For further details, please contact Ascent Research.
