The IL17RB Knockout SK-HEP-1 Polyclonal Cells represent a polyclonal knockout population generated by CRISPR/Cas9-mediated disruption of the IL17RB gene in the SK-HEP-1 human hepatic sinusoidal endothelial cell line. This product provides a heterogeneous loss-of-function model that retains the genetic background and endothelial characteristics of the parental cells, enabling the study of IL17RB without the bias introduced by monoclonal selection. The polyclonal nature ensures improved reproducibility and robustness in functional assays compared to single-cell-derived clones, making it ideal for investigating signal transduction, immune regulation, and drug response.
The parental SK-HEP-1 cell line was established from the ascitic fluid of a patient with liver adenocarcinoma and exhibits dual endothelial and malignant properties, expressing markers such as von Willebrand factor and vascular endothelial cadherin. It serves as a widely accepted in vitro model for hepatic sinusoidal endothelium and hepatocellular carcinoma, facilitating investigations into liver vascular biology, tumor?Cendothelial interactions, and the hepatic microenvironment. The SK-HEP-1 background thus offers a pathophysiologically relevant host for exploring IL17RB function in the context of liver inflammation, fibrosis, and cancer.
The IL17RB gene encodes the receptor for IL-25 (IL-17E), a key mediator of type 2 immune responses. Upon ligand binding, IL17RB recruits the adaptor ACT1 (TRAF3IP2), which engages TRAF6 to activate TAK1 and the IKK complex, ultimately driving NF-??B nuclear translocation and MAP kinase (ERK, JNK, p38) phosphorylation. This signaling cascade induces the expression of Th2 cytokines (IL-4, IL-5, IL-13) and the chemokine CCL20, thereby promoting inflammatory cell recruitment and tissue remodeling. IL17RB thus functions as a critical upstream regulator of pathways implicated in allergic inflammation and epithelial barrier defense.
In SK-HEP-1 cells, IL17RB knockout enables dissection of its role in liver endothelial biology, where IL-25 signaling may contribute to hepatic inflammation, fibrogenesis, and tumor?Cstromal crosstalk. The model is particularly valuable for studying how IL17RB influences endothelial activation, immune cell adhesion, and cytokine production within the liver microenvironment. By eliminating receptor expression, researchers can assess the impact on downstream pathways such as NF-??B and MAPK, and evaluate the potential therapeutic targeting of IL17RB in hepatocellular carcinoma or inflammatory liver diseases.
These IL17RB knockout cells are suited for a wide range of experimental techniques, including western blot analysis of phospho-NF-??B and phospho-MAPKs, RT-qPCR quantification of IL-4, IL-5, and IL-13 transcripts, and ELISA-based measurement of secreted cytokines. Flow cytometry can confirm loss of IL17RB surface expression, while NF-??B luciferase reporter assays provide a functional readout of pathway activity. Co-immunoprecipitation studies enable the investigation of IL17RB?CACT1 interactions, and migration assays can assess the receptor??s role in cell motility. This polyclonal knockout population is an ideal tool for mechanistic studies, drug screening against allergic and inflammatory disorders, and investigation of IL-25/IL17RB axis in liver pathology. For additional information or technical support, please contact Ascent Research.
