The HAVCR1 Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line, in which the HAVCR1 gene has been disrupted by Cas9-mediated gene editing. This polyclonal knockout pool is designed to enable loss-of-function studies of the HAVCR1-encoded protein, TIM-1, across a mixed genetic background that captures population-level heterogeneity. The cellular material is supplied as a ready-to-expand stock for researchers investigating HAVCR1 biology in hepatic cancer models.
The host SK-HEP-1 cell line was originally isolated from the ascitic fluid of a patient with liver adenocarcinoma. Although initially characterized as endothelial, subsequent profiling has established its epithelial origin, and it is now widely adopted as a model system for hepatocellular carcinoma. SK-HEP-1 cells retain key features of hepatic malignancy and are extensively employed for drug screening, tumor biology investigations, and mechanistic studies of liver cancer signaling pathways.
HAVCR1 encodes TIM-1, a type I transmembrane glycoprotein that acts as a receptor for phosphatidylserine (PtdSer) on apoptotic cells and as a portal for hepatitis A virus entry. Engagement of TIM-1 by PtdSer or the co-receptor TIM-4 activates Src family kinases Fyn and Lck, which recruit and phosphorylate the p85 regulatory subunit of PI3K. Downstream signaling proceeds through AKT, MAPK1/3 (ERK1/2), and NF-??B, promoting cell survival, cytokine production, and inflammatory gene expression. Transcriptional control of HAVCR1 is mediated by IL-4, IL-13, TGF-??, cellular stress, and hypoxia. Through these interactions, HAVCR1 integrates signals from apoptotic cell recognition, immune modulation, and viral pathogenesis.
Inactivation of HAVCR1 in the SK-HEP-1 liver adenocarcinoma background eliminates phosphatidylserine-dependent apoptotic cell clearance and disrupts downstream survival and inflammatory cascades. The knockout model is expected to show altered expression of Bcl-2 family members and pro-inflammatory cytokines, along with changes in cell migration and immune evasion properties. Because the cells lack the hepatitis A virus receptor, they also serve as a clean host system for studying alternative viral entry mechanisms or for assessing HAVCR1-dependent infectivity in hepatocellular carcinoma. This polyclonal pool therefore represents a versatile tool for dissecting the role of TIM-1 in hepatocarcinogenesis and therapeutic response.
Typical applications include confirming gene disruption via western blotting, RT-qPCR, and flow cytometry, followed by functional assays such as apoptosis quantification, viral infectivity tests, and migration/invasion experiments. The product is also suitable for phospho-AKT signaling analysis and co-immunoprecipitation of HAVCR1 with interacting proteins like TIM-4 or Src kinases. These methodologies support research into immune checkpoint regulation, drug screening against HAVCR1, and comparative studies of TIM family receptors in liver cancer. For further technical details or inquiries, contact Ascent Research.
