JAG2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of HT29 human colorectal adenocarcinoma cells, harboring targeted disruption of the JAG2 gene. This product is generated through CRISPR/Cas9-mediated gene disruption, producing a heterogeneous pool of cells with loss-of-function mutations in JAG2. The polyclonal format delivers a robust cellular model for studying JAG2-dependent biology without single-cell cloning, maintaining biological diversity while ensuring gene inactivation.
The HT29 parental cell line is a well-established human colorectal adenocarcinoma line exhibiting epithelial morphology. Derived from a primary colon tumor, HT29 cells serve as an intestinal epithelial model for investigating colorectal cancer biology, including differentiation, proliferation, and signaling. These cells retain key intestinal epithelial features, making them valuable for loss-of-function studies of genes involved in colorectal tumorigenesis and cellular homeostasis.
JAG2 encodes Jagged-2, a transmembrane ligand for NOTCH receptors that mediates cell?Ccell communication regulating cell fate, proliferation, and differentiation. Binding to NOTCH1/3 triggers proteolytic cleavages by ADAM10 and gamma-secretase, releasing NICD, which complexes with CSL and MAML1 to activate transcription of targets HES1, HEY1, MYC, and CCND1. JAG2 expression is regulated by E2F transcription factors and TGF-beta pathways, integrating upstream signals to control Notch output. Disruption of JAG2 abolishes ligand-dependent Notch activation, perturbing the JAG2/NOTCH/NICD/CSL/MAML1 signaling axis and downstream transcriptional programs.
In HT29 colorectal cancer cells, JAG2 knockout enables dissection of Notch signaling in intestinal epithelial biology and oncogenesis. Notch pathway dysregulation is common in colorectal cancers, affecting proliferation, stemness, and differentiation. Loss of JAG2 impairs canonical Notch signaling, reducing pro-proliferative targets MYC and CCND1 while potentially promoting differentiation. This model thus allows investigation of ligand-specific Notch contributions to tumorigenicity, metastasis, and therapy resistance, with relevance to colorectal cancer and developmental disorders associated with Notch dysfunction.
JAG2 Knockout HT29 Polyclonal Cells support functional assays including Western blotting for NICD, HES1, and HEY1; RT-qPCR for downstream targets; proliferation assays (MTT/colony formation); migration/invasion assays; and flow cytometry for NOTCH1/3 surface expression. RNA-seq can reveal global transcriptional changes. Applications span Notch pathway studies, drug target validation, and differentiation research. For further information, contact Ascent Research.
