The ABL2 Knockout Huh-7 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 hepatocellular carcinoma line, featuring heterogeneous disruption of the human ABL2 gene. This pooled population harbors loss-of-function mutations that eliminate ABL2 tyrosine kinase expression, offering a genetically diverse model for studying ABL2-dependent processes without monoclonal bias. These polyclonal cells are suited for applications requiring a population-level knockout assessment in a liver cancer background.
The parental Huh-7 line is a well-differentiated hepatocellular carcinoma cell line from a 57-year-old Japanese male patient. It retains hepatocyte characteristics including liver enzyme expression and drug metabolism capacity, while exhibiting tumorigenic properties such as dysregulated proliferation, migration, and invasion. Huh-7 is widely used in liver cancer biology, viral hepatitis research, and pharmacological screening, providing a robust host for CRISPR-based gene disruption.
ABL2 (Arg) is a non-receptor tyrosine kinase that transduces signals from integrins, PDGFR, and EGFR, and is activated by Src kinases and oxidative stress. It phosphorylates the adaptors Crk and CrkL, coupling to the WAVE complex and Arp2/3 to regulate actin polymerization. ABL2 also interacts with F-actin, PSTPIP1, and Abi1, modulating Rac1 and RhoA to control cytoskeletal dynamics, adhesion, and migration. Disruption of ABL2 in this polyclonal model abolishes these molecular interactions, providing a loss-of-function resource for dissecting ABL2 signaling.
In Huh-7 hepatocellular carcinoma, ABL2 contributes to the aggressive phenotype by driving actin remodeling that promotes cell migration and invasion??key steps in metastasis. ABL2 knockout in these cells is expected to impair cytoskeletal reorganization, alter adhesion, and reduce motility, making this model valuable for probing the dependency of liver cancer cells on ABL2 kinase activity and for evaluating the role of ABL2 in metastatic progression.
Representative applications include wound healing and Transwell invasion assays to quantify motility defects, immunofluorescence microscopy to assess actin stress fiber and focal adhesion changes, and Western blotting or co-immunoprecipitation to examine ABL2-mediated phosphorylation of Crk and CrkL. This model also supports kinase inhibitor screening and RT-qPCR profiling of downstream targets such as Rac1 and WAVE/Arp2/3 components. For further information and ordering, please contact Ascent Research.
