The DNMBP Knockout SK-HEP-1 Polyclonal Cells product is a polyclonal population of SK-HEP-1 cells in which the DNMBP gene has been disrupted by CRISPR/Cas9-mediated gene editing. This mixed population of edited cells provides a robust loss-of-function model to study DNMBP-dependent processes without the clonal artifacts that can arise from single-cell-derived lines.
The parental SK-HEP-1 cell line is a human epithelial cell line originally derived from the ascites of a patient with hepatic adenocarcinoma. SK-HEP-1 cells retain key epithelial characteristics and are widely employed as an in vitro model for hepatocellular carcinoma (HCC) research. Their adherent growth and stable epithelial morphology make them particularly suitable for investigating cell polarity, tight junction dynamics, and migration.
DNMBP encodes a multi-domain scaffold protein that functions as a guanine nucleotide exchange factor (GEF) for the small GTPase Cdc42. Mechanistically, DNMBP is activated downstream of receptor tyrosine kinases and phosphatidylinositol 4,5-bisphosphate (PIP2), and it recruits dynamin to sites of endocytosis while simultaneously activating the N-WASP/Arp2/3 complex through Cdc42. This coordination links membrane dynamics to actin nucleation. DNMBP directly interacts with dynamin, N-WASP, syndapin, and F-actin, and it promotes Cdc42-mediated activation of PAK kinases. These interactions position DNMBP at a hub for regulating actin cytoskeleton reorganization, cell polarity establishment, and tight junction assembly.
In the SK-HEP-1 hepatocellular carcinoma background, knockout of DNMBP offers a powerful tool to dissect the role of Cdc42-dependent actin remodeling in cancer cell behavior. Loss of DNMBP function can perturb tight junction integrity, alter cell polarity, and impair directional migration, processes that are frequently dysregulated in metastatic progression. This model enables researchers to investigate how disruption of the DNMBP?CCdc42?CN-WASP axis impacts HCC cell invasiveness and to explore DNMBP as a potential therapeutic target for metastasis.
Typical research applications include using these polyclonal knockout cells in wound healing and Transwell migration/invasion assays to quantify motility changes, as well as in Rho GTPase activation assays to assess Cdc42 activity status. Co-immunoprecipitation experiments can probe altered protein interactions in the absence of DNMBP, while immunofluorescence with phalloidin can visualize F-actin reorganization. Additionally, the model supports drug target validation studies for anti-metastatic agents. For further information or to discuss technical specifications, please contact Ascent Research.
