HIP1R Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population of the human SK-HEP-1 liver adenocarcinoma cell line, enabling loss-of-function studies of the HIP1R gene. This heterogeneous cell pool preserves the genetic diversity of the parental line, making it ideal for population-level analyses of endocytosis, actin regulation, and cancer biology without clonal selection bias.
SK-HEP-1 is an epithelial cell line derived from the ascites of a patient with liver adenocarcinoma. It serves as a robust model for hepatocellular carcinoma, characterized by high invasive and metastatic potential, and is widely used to study tumor progression, drug resistance, and receptor signaling. The introduction of HIP1R knockout in this context adds a powerful tool for dissecting endosomal dysfunction in liver cancer.
HIP1R functions as an adaptor linking clathrin coats to the actin cytoskeleton during clathrin-mediated endocytosis. It interacts with clathrin heavy chain, the AP-2 complex, cortactin, and F-actin, and is regulated upstream by EGFR signaling and huntingtin (HTT). Downstream, it coordinates actin dynamics and dynamin-mediated vesicle scission, thereby modulating receptor internalization and subsequent signaling cascades.
In SK-HEP-1 cells, HIP1R knockout disrupts endocytic trafficking, potentially impairing EGFR internalization and altering downstream pathways that control cell proliferation, apoptosis, and migration??hallmarks of hepatocellular carcinoma. Additionally, HIP1R??s interaction with HTT connects this model to Huntington??s disease mechanisms, offering a platform to study shared pathways between cancer and neurodegeneration.
Researchers can apply this model in Western blotting for HIP1R and clathrin, immunofluorescence for actin and endocytic markers, and flow cytometry for EGFR internalization. Functional assays such as transwell migration, apoptosis induction, and cell viability tests enable studies of drug resistance and cancer cell behavior. The polyclonal format supports robust, reproducible analyses in clathrin-mediated endocytosis and huntingtin-associated research. For further technical details and availability, please contact Ascent Research.
