The EDEM2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma HT29 cell line, featuring targeted disruption of the EDEM2 gene. This loss-of-function model provides a heterogeneous pool for investigating the role of EDEM2 in endoplasmic reticulum-associated degradation (ERAD) and related cellular processes, without clonal selection.
HT29 is an adherent epithelial cell line with mutant APC and p53, widely used as a model for intestinal epithelial biology and colorectal cancer research. Its well-characterized signaling landscape and sensitivity to ER stress make it suitable for studying protein quality control mechanisms in a tumorigenic context.
EDEM2 encodes an ER-resident lectin that recognizes mannose-trimmed N-glycans on misfolded glycoproteins and delivers them to the SEL1L-HRD1 complex for retrotranslocation and proteasomal degradation. EDEM2 is transcriptionally upregulated by the unfolded protein response (UPR) via IRE1??-XBP1, ATF6, and PERK-ATF4 pathways. It interacts with OS9, XTP3-B, and VCP/p97 to facilitate substrate extraction and ubiquitination, thereby mitigating ER stress caused by the accumulation of misfolded glycoproteins.
In HT29 cells, which harbor oncogenic mutations and exhibit elevated basal ER stress, EDEM2 knockout disrupts a key ERAD component. This model enables exploration of how colorectal cancer cells cope with proteotoxic challenges and may reveal synthetic lethal interactions or drug sensitivities related to impaired glycoprotein clearance.
This polyclonal knockout model is suited for assays such as Western blotting for EDEM2 and UPR markers, RT-qPCR for XBP1 splicing and CHOP, flow cytometric viability under ER stress, immunofluorescence for ER morphology, co-immunoprecipitation of EDEM2 interactors, and proteasome activity measurements. Applications span ER stress signaling, glycoprotein quality control, cancer biology, and preclinical drug testing targeting ERAD. For further information, contact Ascent Research.
