The JAG1 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human TE1 esophageal squamous cell carcinoma (ESCC) cell line. This product provides a heterogeneous pool of cells carrying disrupted JAG1 alleles, enabling loss-of-function studies of the Jagged1 ligand in a cancer-relevant setting. The polyclonal format minimizes clonal selection artifacts and is well-suited for population-level functional analyses, preserving natural genetic variability.
The parental TE1 line is a well-established model of human ESCC, originally derived from a primary tumor. TE1 cells exhibit epithelial morphology, retain tumorigenicity in vivo, and recapitulate key molecular features of esophageal cancer. Their extensively characterized genomic landscape makes them an appropriate host for investigating the roles of oncogenic signaling pathways in tumor initiation, progression, and therapeutic resistance.
JAG1 encodes Jagged1, a transmembrane ligand that activates Notch receptors (NOTCH1?C4) upon cell?Ccell contact. Binding triggers sequential cleavage by ADAM17 and the ??-secretase complex (including PSEN1), releasing the Notch intracellular domain (NICD). NICD translocates to the nucleus, where it associates with RBPJ and MAML1 to induce transcription of downstream targets such as HES1, HEY1, and MYC. Jagged1-mediated signaling is modulated by fringe glycosyltransferases (LFNG, MFNG, RFNG) and integrates upstream regulators including HIF1A, TGFB1, WNT3A, and NFKB1. In this knockout model, JAG1 disruption abolishes Jagged1-dependent Notch activation, reduces NICD levels, and impairs expression of effectors that govern cell proliferation, differentiation, and survival.
In ESCC, JAG1 is frequently overexpressed and correlates with aggressive tumor behavior, stem cell maintenance, and chemoresistance. This JAG1 knockout model in TE1 cells enables precise dissection of Jagged1?CNotch signaling contributions to ESCC pathology. Researchers can assess impacts on cellular proliferation, migration, invasion, and crosstalk with Wnt and TGF-?? pathways. The polyclonal nature captures phenotypic diversity and average population responses, better reflecting tumor heterogeneity than clonal lines and facilitating studies of collective cell behavior.
Applications include Notch signaling research, esophageal cancer biology, drug screening for Notch inhibitors, and modeling of Alagille syndrome. The cells are compatible with co-culture Notch activation assays, dual-luciferase Notch reporters, western blotting for JAG1, NICD, and HES1, RT-qPCR of HES1, HEY1, and MYC, flow cytometry, migration and proliferation assays, and drug sensitivity testing using ??-secretase inhibitors. For additional product information or custom requests, please contact Ascent Research.
