This product is a polyclonal SK-HEP-1 HPS5 knockout cell population generated by CRISPR/Cas9-mediated gene disruption. It serves as a loss-of-function model for studying lysosome-related organelle biogenesis. The polyclonal nature retains genetic heterogeneity, suitable for bulk functional assays that reflect population-level responses rather than clonal effects. Researchers can use this model to dissect HPS5-regulated pathways and screen for functional consequences of HPS5 loss across diverse experimental contexts.
SK-HEP-1 is a human hepatic adenocarcinoma cell line derived from ascites of a 52-year-old male with liver adenocarcinoma. It exhibits both endothelial and epithelial characteristics, making it a valuable model for liver cancer and endothelial biology. Commonly used for migration, invasion, and drug sensitivity assays, this cell line provides a robust platform to study oncogenic mechanisms and tumor-endothelial interactions.
HPS5 is an essential subunit of the biogenesis of lysosome-related organelles complex-2 (BLOC-2), which includes HPS3 and HPS6. BLOC-2 cooperates with the AP-3 adaptor complex and clathrin to direct the trafficking of melanosomal proteins such as TYRP1 and PMEL, a process regulated by the small GTPases Rab32 and Rab38. Transcription factors MITF, SOX10, and PAX3 control HPS5 expression, and TGF-beta1 modulates its function. Disruption of HPS5 impairs melanosome maturation and platelet dense granule formation, leading to hypopigmentation and bleeding diathesis characteristic of Hermansky-Pudlak syndrome type 5.
The SK-HEP-1 background, with its mixed endothelial-epithelial phenotype, provides a unique context to study how HPS5 loss affects lysosome-related organelle trafficking in hepatic adenocarcinoma. This model enables investigation of the interplay between BLOC-2 function and tumor processes such as migration and invasion, as well as endothelial-like properties relevant to angiogenesis. Additionally, it offers a system to explore liver-specific effects of BLOC-2 deficiency, including potential roles in hepatic stellate cell activation and fibrosis, making it a versatile tool for both cancer biology and Hermansky-Pudlak syndrome research.
The HPS5 knockout SK-HEP-1 polyclonal cells are ideal for a range of applications, including the molecular characterization of Hermansky-Pudlak syndrome, analysis of melanosome and platelet dense granule biogenesis, and study of lysosomal trafficking in liver cancer. Assays include Western blotting, RT-qPCR, and Sanger sequencing for gene disruption confirmation, immunofluorescence for TYRP1 localization, flow cytometry, and electron microscopy. Migration and drug sensitivity assays can address the role of BLOC-2 in tumor progression. For further information, please contact Ascent Research.
