The AGR2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T-lymphocyte line, with disruption of the AGR2 gene. This loss-of-function model enables investigation of AGR2-dependent processes in a T-cell context, suitable for studies on protein secretion, ER stress, and oncogenic signaling.
Jurkat cells are an immortalized CD4+ T-lymphocyte line from a patient with acute T-cell leukemia, widely used to study TCR signaling, cytokine production, and apoptosis. Their leukemic origin makes them a relevant model for hematopoietic cancers and T-cell biology.
AGR2 is a protein disulfide isomerase that catalyzes disulfide bond formation in the endoplasmic reticulum, critical for protein folding and secretion. It is regulated by ER??, EGFR, TGF-??, IL-1??, and HIF-1??, and promotes secretion of VEGF, MUC1, MUC2, Cathepsin D, and GRP94. AGR2 interacts with EGFR and Cathepsin D, enhancing EGFR-MAPK/ERK signaling to drive proliferation and migration. Additionally, AGR2 associates with BiP and other PDI members in ER quality control. Dysregulation of AGR2 is implicated in breast, prostate, and pancreatic cancers, as well as inflammatory bowel disease, highlighting its role in both oncogenesis and mucosal homeostasis.
In Jurkat T cells, AGR2 knockout permits dissection of its role in cytokine secretion, ER stress, and TCR signaling. Given the leukemic origin, this model is particularly valuable for studying AGR2’s contribution to T-cell leukemia pathogenesis, drug resistance, and EGFR-driven oncogenic pathways. The polyclonal population reflects cellular heterogeneity, enhancing translational relevance for cancer biology and immune function studies. Researchers can explore how loss of AGR2 alters downstream targets such as MUC1 and VEGF, and evaluate changes in ER stress response pathways.
Applications include western blotting and RT-qPCR for AGR2 expression analysis, VEGF secretion assays, ER stress marker quantification (BiP, CHOP), and MTT cell viability assays to assess drug sensitivity. Co-immunoprecipitation validates AGR2-EGFR interactions, while flow cytometry measures surface EGFR levels. Transwell migration assays assess AGR2-dependent cell motility. These tools support research into protein secretion, ER stress, EGFR-MAPK signaling, and T-cell function. For technical inquiries and experimental support, please contact Ascent Research.
