The ANXA1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line. This product enables loss-of-function studies of the ANXA1 gene (annexin A1), which encodes a key anti-inflammatory mediator. The polyclonal format, generated through CRISPR/Cas9-mediated gene disruption, offers a heterogeneous population of cells carrying diverse edits at the ANXA1 locus, providing an accessible model for investigating gene function without clonal selection. Researchers can employ this knockout model to dissect ANXA1??s role in immune regulation and leukemic cell biology.
The Jurkat cell line, originally established from the peripheral blood of a 14-year-old male with acute T cell leukemia, is a widely used model for T cell signaling and acute T cell leukemia research. These suspension cells exhibit a T lymphocyte phenotype and are particularly valuable for studying T cell receptor (TCR)-mediated activation, signal transduction pathways, and apoptosis. The Jurkat host provides a physiologically relevant context for examining ANXA1 function in T cell biology and its impact on leukemic processes.
ANXA1 functions as a potent anti-inflammatory mediator by inhibiting cytosolic phospholipase A2 (cPLA2), thereby suppressing prostaglandin and leukotriene production. Its expression is transcriptionally upregulated by glucocorticoids (dexamethasone, cortisol) and proinflammatory signals like IL-1??, TNF-??, and LPS. Downstream, ANXA1 engages the formyl peptide receptor 2 (FPR2/ALX) and activates ERK and NF-??B pathways. It also interacts with S100A11 and epidermal growth factor receptor (EGFR). These molecular interactions enable ANXA1 to promote phagocytosis of apoptotic cells, regulate caspase-3-mediated apoptosis, and modulate cell migration and proliferation.
In the Jurkat T cell leukemia context, disruption of ANXA1 alters critical cellular processes. Knockout cells can reveal how ANXA1 modulates TCR signaling, the MAPK/ERK and NF-??B pathways, and apoptotic programs in leukemic T cells. This model is particularly valuable for investigating ANXA1??s dual roles in cancer??where it may suppress tumor growth via pro-apoptotic effects or, conversely, promote invasion and metastasis. The polyclonal population captures diverse gene disruptions, making it suitable for studying heterogeneous responses in leukemia biology.
This ANXA1 knockout model supports advanced applications such as mechanistic studies of inflammation resolution, T cell signaling, and cancer cell invasion. Standard assays including western blotting, RT-qPCR, immunofluorescence, and flow cytometry enable detailed expression and phenotypic analysis. Functional assays like apoptosis and migration assays can characterize ANXA1-dependent processes. The model is also applicable to drug screening for anti-inflammatory agents and targeted leukemia therapies. For additional technical details, please contact Ascent Research.
