The KDELR1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the KDELR1 gene. Derived from the SK-HEP-1 hepatic adenocarcinoma line, this heterogeneous product enables loss-of-function studies without clonal isolation, providing a robust model for population-level analysis.
SK-HEP-1 cells originate from ascitic fluid of a hepatocellular carcinoma patient and exhibit both epithelial and mesenchymal traits plus endothelial features. This unique phenotype makes them a valuable platform for investigating liver cancer progression, endothelial mimicry, and epithelial-mesenchymal transition.
KDELR1 functions as a retrieval receptor for ER-resident proteins carrying the C-terminal KDEL sequence. It binds ligands like BiP, calreticulin, and PDI in the Golgi and sorts them into COPI vesicles through associations with ARF1 and coatomer subunits (??-COP, ??-COP). Upstream, KDELR1 is transcriptionally regulated by UPR factors ATF6, XBP1, and ATF4 in response to ER stress. Downstream, its activity maintains ER chaperone pools; knockout depletes these factors, triggering constitutive ER stress and UPR activation. This retrograde cycle is essential for ER homeostasis and secretory pathway fidelity.
In SK-HEP-1 liver cancer cells, KDELR1 knockout impairs ER protein quality control, inducing chronic ER stress that may influence tumor survival, secretory output, and metastatic potential. This system is particularly relevant for dissecting how ER-Golgi trafficking perturbations promote hepatocellular carcinoma phenotypes and for studying interactions with the tumor microenvironment. Beyond liver cancer, this model is valuable for research into liver fibrosis, ER storage diseases, and viral protein processing that depend on intact ER retrieval mechanisms.
The KDELR1 Knockout SK-HEP-1 Polyclonal Cells support diverse applications in ER stress biology and liver cancer research. They enable monitoring of UPR activation via Western blot or ERSE-luciferase assays, analysis of secretory trafficking by immunofluorescence and flow cytometry, and evaluation of metastatic behavior using transwell assays. This model is also suitable for drug screening with tunicamycin sensitivity tests and co-immunoprecipitation of COPI interactions. For inquiries, contact Ascent Research.
