Genome-edited Cells
Liver
The USP20 Knockout Huh-7 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human hepatocellular carcinoma Huh-7 line. It enables loss-of-function studies of USP20, a deubiquitinase that stabilizes key signaling factors including ??-catenin and HIF-1??, thereby modulating Wnt, NF-??B, hypoxia, and autophagy pathways. This product is ideal for investigating USP20's role in liver cancer pathogenesis, deubiquitinase biology, and drug target validation, using applications such as reporter assays, co-immunoprecipitation, and phenotypic profiling. It provides a precise genetic tool for hepatocellular carcinoma research.
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FZD7 Knockout HEK293T Cell Line
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The USP20 Knockout Huh-7 Cell Line is a CRISPR/Cas9-edited human liver cancer cell line designed to ablate ubiquitin-specific protease 20 (USP20), generating a stable loss-of-function model. Quality-controlled for consistent knockout, it ensures reliable USP20 protein deficiency across passages, enabling precise functional studies in hepatocellular carcinoma (HCC) without the variability of transient knockdown methods.
The parental Huh-7 cell line was established from a hepatocellular carcinoma of a 57-year-old Japanese male and exhibits epithelial morphology. This widely used HCC model retains key tumorigenic features, including dysregulated proliferation, metabolic reprogramming, and sensitivity to hypoxic stress. Huh-7 cells are permissive for hepatitis C virus replication, extending their utility to viral hepatocarcinogenesis research. The well-characterized background makes this USP20 knockout derivative directly applicable to mechanistic and translational liver cancer studies.
USP20 is a deubiquitinase that cleaves K48- and K63-linked polyubiquitin chains from substrates, regulating protein stability and signal transduction. It is activated by hypoxia and inflammatory stimuli such as TNF-??, and directly deubiquitinates HIF-1??, ??-catenin, TRAF6, RIPK1, and ULK1. USP20-mediated stabilization of HIF-1?? amplifies hypoxia-driven gene expression; deubiquitination of ??-catenin potentiates Wnt/TCF/LEF transcriptional activity; and modification of TRAF6 and RIPK1 regulates the NF-??B pathway via the IKK?CI??B???Cp65 axis. Additionally, USP20 controls autophagy initiation by targeting ULK1 within the ULK1?CATG13?CFIP200 complex.
In the Huh-7 hepatocellular carcinoma context, USP20 disruption is particularly significant because USP20 may foster liver tumorigenesis by stabilizing oncogenic ??-catenin and HIF-1??. Both factors are commonly dysregulated in HCC and contribute to malignant properties. This knockout cell line allows direct assessment of USP20’s role in proliferation, apoptotic resistance, migration, and autophagy, offering a platform to identify USP20-dependent vulnerabilities for therapeutic exploitation.
Research applications include co-immunoprecipitation and ubiquitination analyses to study USP20 substrates, dual-luciferase reporter assays for Wnt or NF-??B activity, and phenotypic characterization via viability, apoptosis, and migration/invasion tests. The line supports HIF-1?? reporter measurements under hypoxia, autophagy flux monitoring, and small-molecule inhibitor screening. These tools facilitate target validation and deubiquitinase research in liver cancer. For further details, please contact Ascent Research.
