The JAGN1 Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population targeting the JAGN1 gene in the HT29 human colorectal adenocarcinoma cell line. This polyclonal format provides a heterogeneous pool of cells with disrupted JAGN1 function, enabling loss-of-function studies without clonal selection bias, and is suited for assessing gene disruption effects across a dynamic cellular population in an epithelial context.
HT29 cells are a well-characterized epithelial cell line derived from a primary colorectal adenocarcinoma. They retain intestinal epithelial characteristics, including the ability to differentiate into enterocyte-like cells and produce mucins, and are widely employed in colorectal cancer research, drug absorption studies, and investigations of intestinal epithelial cell biology. Their epithelial morphology and robust growth make them an excellent host for studying endoplasmic reticulum (ER)-related processes.
JAGN1 encodes an ER-resident protein essential for ER homeostasis and neutrophil biology. It interacts with oligosaccharyltransferase subunits such as STT3A and ER chaperones like HSPA5/BiP, and is critical for N-glycosylation and granulocyte differentiation. JAGN1 functions downstream of CSF3 (G-CSF) and is regulated by ER stress sensors ATF6 and IRE1, linking it to the ATF6-XBP1-HSPA5 signaling axis. Its loss impairs the maturation of neutrophil granular proteins, including ELANE, and triggers ER stress responses that disrupt protein folding and quality control mechanisms.
In the HT29 background, JAGN1 knockout provides a valuable model for dissecting ER stress signaling and N-glycosylation pathways in epithelial cells, with direct relevance to colorectal cancer progression. ER stress is a hallmark of many solid tumors, and HT29 cells offer a platform to investigate how loss of JAGN1 alters glycoprotein synthesis, stress adaptation, and cell survival. While JAGN1 is physiologically linked to neutrophil function, its broadly conserved role in ER biology enables translational studies into cancer cell resilience and immune-related defects.
These polyclonal knockout cells are ideal for neutropenia disease modeling, ER stress research, and colorectal cancer studies. Typical assays include western blotting for JAGN1, RT-qPCR for ER stress markers (HSPA5, DDIT3), ER stress induction with tunicamycin, immunofluorescence for ER morphology, and flow cytometry with annexin V/PI for viability. RNA-seq transcriptomic analysis further supports mechanistic investigations. For drug screening targeting neutrophil disorders or ER stress pathways, this model offers a physiologically relevant tool. For further details, please contact Ascent Research.
