The DPYSL5 Knockout SK-HEP-1 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. This polyclonal pool carries targeted disruptions of the DPYSL5 gene, creating a loss-of-function model for studying the collapsin response mediator protein 5 (CRMP5).
SK-HEP-1 was originally established from ascites of a patient with liver adenocarcinoma. These cells exhibit a hybrid endothelial/epithelial phenotype, co-expressing markers such as von Willebrand factor, CD34, and CK-18, and are widely used as an in vitro model of hepatic sinusoidal endothelium. Their functional properties, including tube formation, migration, and angiogenic responsiveness, make them a standard platform for tumor angiogenesis and hepatocellular carcinoma research.
DPYSL5 encodes CRMP5, a cytosolic phosphoprotein that integrates guidance cues to regulate microtubule dynamics and growth cone collapse. CRMP5 functions downstream of semaphorin-3A (Sema3A) binding to neuropilin-1/plexin-A receptor complexes, becoming phosphorylated by Cdk5 and GSK-3??. This phosphorylation reduces its affinity for tubulin, triggering microtubule destabilization and cytoskeletal retraction. CRMP5 also participates in neurotrophin (NGF, BDNF) pathways and cross-talks with RhoA/Rac1-mediated actin remodeling. Furthermore, CRMP5 forms heterotetramers with CRMP1, CRMP2, and CRMP4, modulating their activities and expanding signal integration.
In SK-HEP-1 cells, which possess robust endothelial-like characteristics, CRMP5 is poised to control cytoskeletal organization underlying angiogenesis, migration, and barrier function. Aberrant CRMP5 expression has been associated with hepatocellular carcinoma progression and with paraneoplastic neurological syndromes, where anti-CRMP5 autoantibodies serve as diagnostic markers. Disruption of DPYSL5 in this hepatic endothelial model thus enables dissection of CRMP5-dependent contributions to tumor angiogenesis, cancer cell invasion, and endothelial plasticity.
Applications of this polyclonal DPYSL5 knockout pool include semaphorin-induced growth cone collapse assays, liver cancer metastasis studies, and paraneoplastic autoantibody screening. Researchers can employ tube formation assays to assess angiogenic capacity, transwell migration assays to evaluate motility, and immunofluorescence to visualize microtubule networks. Co-immunoprecipitation experiments can probe CRMP5 interactions with tubulin and CRMP partners, while kinase inhibitor screens can target GSK-3?? or Cdk5. Drug sensitivity profiling may reveal therapeutic vulnerabilities. For further information, please contact Ascent Research.
