The DYNC1LI1 Knockout SK-HEP-1 Polyclonal Cells constitute a population of SK-HEP-1 cells subjected to CRISPR/Cas9-mediated disruption of the DYNC1LI1 gene, providing a loss-of-function model for investigating cytoplasmic dynein 1 light intermediate chain function. This polyclonal knockout product retains the genetic heterogeneity inherent to CRISPR-edited pools, making it suitable for studies where clonal variation is not a primary concern and bulk cellular responses are of interest.
The host cell line, SK-HEP-1, is a human hepatic adenocarcinoma-derived cell line that exhibits an endothelial-like phenotype, expressing endothelial markers and displaying angiogenic potential. Widely employed as a liver sinusoidal endothelial model, SK-HEP-1 cells are valuable for research into endothelial cell biology, drug transport across liver endothelium, and tumor microenvironment interactions.
DYNC1LI1 encodes a light intermediate chain subunit of the cytoplasmic dynein 1 motor complex, which functions as a microtubule minus-end-directed transporter. It directly interacts with the dynactin complex (including p150Glued/DCTN1), the regulatory proteins LIS1 (PAFAH1B1), NDE1, NDEL1, and the adaptor BICD2, as well as HOOK3 and FIP1C, to mediate the retrograde movement of diverse cargoes. Through these interactions, DYNC1LI1 contributes to signaling endosome transport, lysosomal positioning, mitochondrial distribution, and timely inactivation of the mitotic checkpoint. It also participates in autophagy and ciliogenesis, with disruptions linked to neurodevelopmental disorders, motor neuron disease, and cancer progression.
In the context of SK-HEP-1 cells, knockout of DYNC1LI1 is expected to impair dynein-dependent intracellular trafficking, potentially altering organelle localization, cell polarization, and migratory behavior. Given the endothelial-like properties of this cell line, the model is particularly relevant for examining how retrograde transport governs angiogenesis, endothelial barrier function, and transcytosis. It also provides a platform to explore dynein-related pathological mechanisms in hepatic cancer and neurodevelopmental disorders, where DYNC1LI1 has been implicated.
Researchers can apply this knockout model in a variety of assays to dissect dynein-mediated processes. Western blotting and immunofluorescence enable confirmation of protein loss and visualization of organelle markers, while live-cell tracking of lysosomes and flow cytometric endocytosis assays quantify alterations in organelle dynamics and uptake. Functional studies such as scratch wound migration and Transwell invasion assays evaluate cell motility and invasiveness, and co-immunoprecipitation permits mapping of DYNC1LI1 interaction networks. This polyclonal population is also suitable for drug transport and toxicity screens, autophagy flux analyses, and investigations of mitotic spindle assembly in endothelial-like contexts. For additional information or to acquire this product, please contact Ascent Research.
