The HAVCR1 Knockout 143B Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population derived from the 143B human osteosarcoma cell line, engineered for targeted disruption of the HAVCR1 gene. This polyclonal knockout model provides a heterogeneous pool of gene-edited cells, enabling robust loss-of-function studies without clonal selection artifacts. The product is designed to support high-resolution investigations into HAVCR1-dependent signaling networks and viral entry mechanisms in a bone cancer context.
The 143B cell line is a well-characterized subclone of HOS, originally isolated from a primary osteosarcoma. As an adherent, epithelial-like human bone cancer model, 143B cells are widely employed to study osteosarcoma pathogenesis, metastasis, and therapeutic vulnerabilities. Their established genetic and phenotypic stability makes them a reliable host for CRISPR-based functional genomics, particularly in exploring genes involved in tumor progression and immune modulation.
HAVCR1, also known as TIM-1, encodes a transmembrane receptor that binds phosphatidylserine and serves as a cellular entry gate for the hepatitis A virus. Its signaling is triggered by upstream mediators including IL-4, IL-13, and viral capsid proteins. HAVCR1 directly interacts with the regulatory subunit PIK3R1 and the ligand TIM-4, subsequently activating downstream effectors AKT and ERK1/2 through the PI3K-AKT and ERK/MAPK cascades. These pathways (HAVCR1 ?? PIK3R1 ?? AKT; HAVCR1 ?? ERK/MAPK) drive cell survival, proliferation, and viral internalization, linking HAVCR1 to both immune regulation and oncogenic processes.
In the 143B osteosarcoma background, HAVCR1 knockout abrogates these pro-survival and proliferative signals, potentially attenuating tumorigenicity and altering susceptibility to immune checkpoint modulation. Furthermore, loss of the viral receptor renders the cells resistant to hepatitis A virus infection, establishing a unique platform to dissect virus-host interactions and receptor-mediated entry in a bone tumor microenvironment. This model is particularly valuable for investigating how HAVCR1-associated pathways intersect with cancer cell signaling.
This knockout cell population facilitates diverse applications, including hepatitis A virus infection assays, cancer drug screening, and immune regulation studies. Researchers can employ complementary techniques such as flow cytometry for receptor expression profiling, western blotting for pathway activation analysis, and functional assays for proliferation, apoptosis, and migration. By linking HAVCR1-mediated signaling to specific phenotypes, this model accelerates discovery in oncology and virology. For further information, please contact Ascent Research.
