The DNM1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited pool of SK-HEP-1 human liver adenocarcinoma cells with disrupted DNM1 expression. As a polyclonal knockout population, this model avoids clonal selection artifacts and provides a heterogeneous loss-of-function system for dynamin-1 research. It is suitable for rapid generation of knockout cells without single-cell cloning, facilitating endocytosis and signaling studies.
SK-HEP-1 is a well-characterized cell line derived from ascites of a male patient with hepatic adenocarcinoma and exhibits both hepatic and endothelial-like features. Widely used in cancer biology, the line supports robust clathrin-mediated endocytosis and expresses key endocytic machinery, making it an appropriate host for investigating DNM1 function in a non-neuronal context.
DNM1 encodes dynamin-1, a large GTPase that assembles into helical polymers at the necks of clathrin-coated pits and drives membrane fission upon GTP hydrolysis. This process is critical for receptor internalization and signal attenuation. Dynamin-1 activity is modulated by growth factor signaling and calcium flux, and it interacts with amphiphysin (AMPH), endophilin (SH3GL2), synaptojanin (SYNJ1), clathrin heavy chain (CLTC), and the AP2A1 adaptor complex to coordinate vesicle scission and uncoating, thereby controlling the endocytic downregulation of activated receptors.
In SK-HEP-1 cells, DNM1 knockout is expected to impair clathrin-dependent endocytosis, leading to altered receptor trafficking and sustained signaling. The endothelial-like properties of the host line allow investigation of dynamin-1??s role in transendothelial migration, vascular mimicry, and tumor cell invasion, linking endocytic defects to liver adenocarcinoma progression.
Applications include quantitative transferrin uptake assays, immunofluorescence visualization of endocytic structures, co-immunoprecipitation of dynamin complexes, and Western blot confirmation of knockout. The cells are suitable for receptor internalization studies, rescue experiments, and screening of endocytosis inhibitors. This model also supports research on cancer cell migration and dynamin-related neurological disorders. For further details, please contact Ascent Research.
