The JAG2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Jurkat T-lymphocyte cell line. These cells carry a targeted disruption of the JAG2 gene, leading to ablation of the Notch ligand Jagged-2. The polyclonal nature preserves the spectrum of editing outcomes across the cell pool, avoiding clonal selection artifacts, and provides a versatile loss-of-function model for investigating JAG2-dependent signaling pathways.
The Jurkat cell line was established from the peripheral blood of a 14-year-old male with relapsed acute T-cell leukemia (T-ALL). As an immortalized T-lymphoblast model, it has been widely employed to study T-cell receptor signaling, apoptosis, and leukemic transformation. Jurkat cells express T-cell lineage markers and harbor oncogenic mutations, making them particularly relevant for Notch pathway research in the context of T-ALL.
JAG2 encodes Jagged-2, a DSL family ligand that activates Notch signaling by binding NOTCH1?C4 receptors. Ligand engagement triggers ADAM10/17 and ??-secretase cleavages, releasing the Notch intracellular domain (NICD). NICD complexes with the DNA-binding factor CSL/RBPJ and coactivator MAML to transactivate target genes such as HES1, HEY1, and MYC. Fringe glycosyltransferases and the E3 ubiquitin ligase MIB1 modulate ligand-receptor interactions, while upstream GATA and RUNX transcription factors control JAG2 expression. Downstream effectors include NF-??B and CCND1, linking Notch to cell proliferation and survival.
In Jurkat T-ALL cells, oncogenic Notch signaling often stems from NOTCH1 mutations. JAG2 knockout dissects ligand-dependent versus receptor-intrinsic contributions. Removing Jagged-2 abolishes potential autocrine or paracrine Notch loops, enabling precise examination of altered HES1 and MYC expression and its crosstalk with TCR pathways in T-cell leukemogenesis.
These cells are applicable to co-culture signaling assays, dual-luciferase reporter systems, and RT-qPCR for HES1 or HEY1 transcripts. Functional validation by flow cytometry and NICD Western blotting are routinely employed. Primary applications include T-ALL disease modeling, Notch inhibitor screening, and investigating Notch modulation in adoptive T-cell therapy. For further information, contact Ascent Research.
