The GPD1L Knockout SK-HEP-1 Polyclonal Cells product comprises a polyclonal population of SK-HEP-1 cells harboring a CRISPR/Cas9-mediated disruption of the endogenous GPD1L gene. This genetically engineered model enables loss-of-function studies of GPD1L within a heterogeneous hepatic adenocarcinoma background, offering a powerful tool for investigating the multifaceted roles of GPD1L in cardiac ion channel regulation and cancer cell metabolism.
SK-HEP-1 is a human liver adenocarcinoma cell line that uniquely co-expresses epithelial and endothelial markers, making it a versatile platform for hepatic oncology, metastasis, and vascular biology research. Derived from a patient with liver adenocarcinoma, these cells exhibit robust in vitro growth and have been widely utilized to study drug metabolism, tumor cell migration, and endothelial-like characteristics. The SK-HEP-1 background provides a relevant cellular context for exploring GPD1L functions in liver cancer, complementing its established cardiac roles.
GPD1L encodes a protein that critically modulates the cardiac sodium channel Nav1.5 (SCN5A) by regulating its trafficking to the plasma membrane, likely through interactions involving the glycerol-3-phosphate shuttle. It forms complexes with SCN5A, ankyrin-G, and syntrophin to ensure proper channel localization. Downstream, GPD1L controls SCN5A-mediated sodium current, impacting cardiac action potential conduction. Pathway components linking GPD1L to electrophysiology include SCN5A, SCN1B, CACNA1C, and KCNH2.
In the context of SK-HEP-1 cells, disrupting GPD1L establishes a unique model to interrogate its potential non-cardiac functions, particularly in hepatic cancer metabolism. Although GPD1L is best known for its role in Brugada syndrome and sudden infant death syndrome, emerging evidence suggests its involvement in metabolic reprogramming of cancer cells. By ablating GPD1L in this hepatic adenocarcinoma background, researchers can dissect its impact on cellular bioenergetics, redox balance, and ion channel-mediated signaling pathways that may influence tumorigenesis and metastasis. This model thus bridges cardiac and cancer biology, enabling studies on how GPD1L coordinates metabolic and electrophysiological processes across distinct cellular milieus.
This polyclonal knockout model is ideal for diverse assays, including immunofluorescence and Western blotting to assess SCN5A localization, patch-clamp electrophysiology for sodium current analysis, and metabolic flux studies. In oncology, it supports proliferation, migration, and invasion assays to evaluate GPD1L’s role in liver cancer aggressiveness. RNA-sequencing can further delineate GPD1L-dependent transcriptomic changes. For ordering information or technical inquiries, please contact Ascent Research.
