The IRGQ Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast cancer cell line, featuring targeted disruption of the interferon-inducible GTPase IRGQ gene. This pooled knockout model offers a genetically heterogeneous loss-of-function system for investigating IRGQ-dependent mechanisms in a physiologically relevant epithelial context.
The T-47D host cell line was originally established from the pleural effusion of a 54-year-old female with metastatic ductal carcinoma. These cells are estrogen receptor-positive, progesterone receptor-positive, and lack HER2 overexpression, classifying them as a luminal A breast cancer model. They retain hormone responsiveness and serve as a well-characterized platform for studying hormone signaling, autophagy, and immune-related processes in breast cancer.
IRGQ is an interferon-inducible GTPase that functions downstream of the IFN-gamma receptor, activated via the JAK/STAT pathway and transcriptionally regulated by STAT1 and IRF1. It localizes to pathogen-containing vacuoles and facilitates autophagy-mediated clearance by interacting with core autophagy machinery, including ATG5, BECN1, and LC3 (ATG8 family members). IRGQ promotes autophagosome formation, thereby bridging innate immune signaling to selective degradation of intracellular cargo and playing a critical role in host defense.
In the T-47D luminal A breast cancer background, IRGQ knockout enables dissection of autophagy-dependent immune evasion and tumor cell-autonomous innate immunity. Because T-47D cells are hormone-responsive and representative of a common breast cancer subtype, this model is particularly valuable for exploring how interferon and autophagy pathways intersect to modulate MHC-I expression, cytokine responses, and autophagic flux under pro-inflammatory conditions.
Researchers can apply these polyclonal knockout cells in a range of assays, including western blotting for LC3-II, RT-qPCR for IRGQ, immunofluorescence for IRGQ localization, autophagy flux assays using chloroquine, co-immunoprecipitation with ATG proteins, flow cytometry for MHC-I, and interferon-gamma stimulation experiments. Typical research areas encompass innate immune response in breast cancer, autophagy regulation, host-pathogen interactions, and tumor immunology. For additional technical information, please contact Ascent Research.
