The IVNS1ABP Knockout SK-HEP-1 Polyclonal Cells consist of a heterogeneous population of SK-HEP-1 cells that have undergone CRISPR/Cas9-mediated disruption of the IVNS1ABP gene, yielding a mixed knockout model rather than a clonal isolate. This polyclonal format is advantageous for studies requiring genotypic diversity while preserving loss-of-function effects across the culture. The target gene encodes a protein that negatively regulates RELA/p65 and organizes the actin cytoskeleton, making these cells a valuable tool for investigating IVNS1ABP-dependent pathways.
The parental SK-HEP-1 line originates from the ascites of a 52-year-old male with liver adenocarcinoma and exhibits both epithelial and endothelial-like characteristics. This dual phenotype has established SK-HEP-1 as a robust model for hepatic cancer biology, drug metabolism studies, and investigations of endothelial-like cell behavior. The knockout derivative retains this background, enabling dissection of IVNS1ABP function specifically within a liver adenocarcinoma context.
IVNS1ABP functions as a negative regulator of NF-??B signaling by directly binding the RELA/p65 subunit and dampening its transcriptional activity. It also interacts with F-actin, thereby regulating actin cytoskeleton organization, and is involved in antiviral responses through its binding to the influenza virus NS1 protein. Upstream regulators such as TNF-??, IL-1??, and NS1 can modulate IVNS1ABP activity, while downstream targets include IL-6, CCL2, NFKBIA, and ACTB reorganization. These molecular interactions place IVNS1ABP at the nexus of immune signaling, cytoskeletal dynamics, and viral infection.
In the SK-HEP-1 background, CRISPR-mediated knockout of IVNS1ABP relieves its inhibitory effect on RELA/p65, leading to enhanced NF-??B transcriptional activity. This can result in elevated expression of pro-inflammatory cytokines such as IL-6 and CCL2, and may promote cell migration via altered actin dynamics. Given the endothelial-like properties of the host cells, this model is particularly suited for studying how loss of IVNS1ABP influences the metastatic potential of liver adenocarcinoma and its interplay with the immune microenvironment.
These polyclonal knockout cells are applicable to a variety of experiments, including NF-??B luciferase reporter assays, western blotting for RELA and phospho-RELA, immunofluorescence staining of F-actin, and scratch wound healing assays to assess motility. They facilitate research on NF-??B regulatory mechanisms, influenza virus-host interactions involving NS1, and cancer cell invasion. For further technical support or product information, please contact Ascent Research.
