The ACTR5 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from SK-HEP-1, a human hepatic adenocarcinoma cell line. This product enables loss-of-function analysis of ACTR5, a gene encoding an essential subunit of the INO80 chromatin remodeling complex. The polyclonal format offers a heterogeneous mixture of gene-edited cells, facilitating robust and reproducible studies of ACTR5 deficiency without the biases of clonal selection.
SK-HEP-1 cells were originally isolated from the ascites of a patient with liver adenocarcinoma and are widely used as a model for hepatic cancer research. This cell line exhibits epithelial morphology and retains many characteristics of hepatocellular carcinoma, including dysregulated signaling pathways relevant to hepatocarcinogenesis. The SK-HEP-1 background provides a physiologically relevant hepatic context for investigating chromatin remodeling functions in liver cancer biology.
ACTR5 is a core subunit of the multi-subunit INO80 ATP-dependent chromatin remodeling complex, which modulates nucleosome positioning to regulate transcription, DNA repair, and replication. Within this complex, ACTR5 interacts directly with INO80, RUVBL1, RUVBL2, ACTR8, and ACTR6 to coordinate ATP hydrolysis-driven nucleosome sliding and eviction. The INO80 complex is recruited to chromatin by DNA damage signals and cell cycle regulators, including E2F transcription factors, and modulates the expression of downstream DNA repair genes, cell cycle genes, and Wnt pathway targets. Consequently, ACTR5 deficiency disrupts chromatin dynamics, compromising transcriptional regulation, genome stability, and DNA damage response pathways.
In SK-HEP-1 hepatocellular carcinoma cells, ACTR5 knockout likely impairs the INO80 chromatin remodeling activity, leading to altered gene expression programs and defective DNA repair. Given the role of chromatin remodelers in liver cancer progression, this model provides a valuable tool to dissect the contribution of INO80-dependent chromatin remodeling to hepatocarcinogenesis. The loss of ACTR5 may sensitize cells to genotoxic stress or modulate Wnt/??-catenin signaling, both critical in liver tumor biology. Thus, the ACTR5 polyclonal knockout pool is particularly suited for investigating how chromatin dysregulation contributes to hepatocellular carcinoma and for testing therapeutic strategies targeting epigenetic vulnerabilities.
This product is designed for a wide range of applications, including dissecting INO80 complex function in DNA damage repair using ??H2AX immunofluorescence and comet assays, analyzing cell cycle distribution via flow cytometry, and profiling transcriptional changes by RNA-seq. Additionally, it serves as a platform for liver cancer drug screening, where ACTR5 loss may reveal synthetic lethal interactions or enhance sensitivity to chemotherapeutics. The polyclonal nature minimizes clonal effects, enabling robust assessment of phenotype penetrance. For further information or custom inquiries, please contact Ascent Research.
