The DYNLT3 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the DYNLT3 gene within the human SK-HEP-1 hepatocellular carcinoma background. This polyclonal format provides a genetically heterogeneous loss-of-function model suitable for studying DYNLT3-dependent processes without clonal artifacts. By introducing CRISPR/Cas9-mediated gene disruption, the product enables investigation of cytoplasmic dynein light chain function in a liver cancer context, offering a robust tool for dissecting intracellular transport and mitotic regulation.
SK-HEP-1 is a well-characterized human liver adenocarcinoma-derived epithelial cell line widely employed in hepatic cancer biology research. Originating from a patient with adenocarcinoma, these cells exhibit morphological and molecular features of liver epithelial tumors, facilitating studies in hepatocellular carcinoma pathogenesis, drug response, and cellular signaling. The epithelial origin and adherent growth properties of SK-HEP-1 make it amenable to imaging-based assays, biochemical analyses, and functional genomic screens, ensuring compatibility with diverse experimental workflows.
DYNLT3 encodes a non-catalytic dynein light chain subunit that is essential for cargo binding and regulation of cytoplasmic dynein motor activity. Mechanistically, DYNLT3 interacts with core dynein components such as DYNC1H1 and adaptor proteins including DCTN1, NDE1, NDEL1, and PAFAH1B1 to mediate vesicular and organelle transport along microtubules. Its activity is regulated by upstream kinases CDK1 and PLK1, which phosphorylate dynein-associated factors to coordinate mitotic spindle organization and cell cycle progression. Disruption of DYNLT3 uncouples these regulatory circuits, impairing dynein-dependent processes and providing insight into the molecular choreography of mitosis and intracellular trafficking.
In the context of hepatocellular carcinoma, altered DYNLT3 expression has been associated with tumorigenic phenotypes, making the SK-HEP-1 knockout model particularly relevant for exploring how dysregulated dynein function contributes to cancer biology. The polyclonal knockout population permits assessment of loss-of-function effects on mitotic fidelity, cell cycle distribution, and cell migration, which are critical for understanding liver cancer progression. By linking dynein machinery to oncogenic signaling, this model enables dissection of pathways that may distinguish normal epithelial physiology from malignant transformation.
This knockout cell product is designed for a broad spectrum of research applications, including the analysis of dynein-mediated intracellular transport, mitotic spindle dynamics, and cell cycle regulation in hepatic cancer models. Representative experimental approaches include western blotting to assess dynein complex integrity, immunofluorescence microscopy to visualize spindle abnormalities, live-cell imaging of cargo movement, flow cytometric cell cycle profiling, and migration assays. These tools support mechanistic studies of cargo adaptor interactions, kinase-dependent regulation, and tumor cell behavior. For further details or custom requests, please contact Ascent Research.
