The JAG2 Knockout UM-UC-3 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population in which the JAG2 gene has been disrupted. This pool of UM-UC-3 cells lacks Jagged2 ligand expression, providing a loss-of-function model for investigating JAG2-dependent functions. As a polyclonal population, it reflects diverse editing events, avoiding clonal selection bias and making it suitable for population-level studies.
UM-UC-3 is a human bladder transitional cell carcinoma line isolated from a primary tumor. It is a well-established in vitro model for bladder cancer, exhibiting invasive behavior and expressing components of the Notch pathway, which makes it relevant for studying ligand-mediated signaling in this malignancy.
Jagged2 is a transmembrane Notch ligand that activates NOTCH1 and NOTCH3 receptors. Binding leads to proteolytic cleavage by ADAM10 and gamma-secretase, releasing NICD. NICD forms a complex with CSL (RBPJ) and MAML to drive transcription of HES1, HEY1, MYC, CCND1, and BCL2. JAG2 is regulated by E2F, NF-??B, Wnt/??-catenin, TGF-??, and HIF-1??. The ligand interacts with MIB1 and DLL1. Knockout of JAG2 abolishes Jagged2-mediated Notch activation, reducing NICD and target gene expression, thereby impairing Jagged2-dependent signaling.
In the UM-UC-3 bladder cancer context, JAG2 disruption allows precise analysis of Jagged2-Notch signaling contributions to tumor cell proliferation, survival, and stemness. This model is valuable for distinguishing Jagged2-specific functions from those of other Notch ligands and for examining pathway dependencies in a clinically relevant setting. It also enables study of crosstalk with Wnt and TGF-?? pathways.
This polyclonal knockout cell population is ideal for Western blotting of NICD and HES1, RT-qPCR for Notch targets, RNA-seq profiling, MTS proliferation assays, Boyden chamber migration/invasion assays, and sphere formation. Flow cytometry and co-culture with Notch reporters are also applicable. The cells support drug target validation, combination therapy studies, and tumor microenvironment research. For further information, contact Ascent Research.
