The EFCAB14 Knockout SK-HEP-1 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatic adenocarcinoma cell line. This product features a targeted disruption of the EFCAB14 gene, achieved through CRISPR/Cas9-mediated gene editing, resulting in a heterogeneous pool of cells with loss-of-function mutations. As a polyclonal population, it represents a versatile tool for studying gene function without single-cell cloning, enabling the analysis of mixed genotypes that may better recapitulate tumor heterogeneity. The knockout model serves as a reliable platform for investigating EFCAB14-dependent cellular processes in liver cancer biology.
The host cell line, SK-HEP-1, is a well-established human hepatic adenocarcinoma epithelial cell line originally isolated from the ascites of a male patient with liver adenocarcinoma. SK-HEP-1 cells exhibit a unique biphasic phenotype combining both endothelial and epithelial characteristics, making them particularly valuable for studying liver tumorigenesis and the interplay between mesenchymal and epithelial features in cancer progression. This dual nature allows researchers to examine how calcium signaling pathways, modulated by EFCAB14, may influence both cellular adhesion and motility, processes critical for tumor invasion and metastasis.
EFCAB14 encodes a calcium-binding protein containing EF-hand domains, which are known to undergo conformational changes upon binding intracellular Ca2+. This protein is implicated in calcium signal transduction, where it likely functions downstream of transient intracellular Ca2+ elevation and the Ca2+/calmodulin-dependent kinase CaMKII. EFCAB14 may interact with calmodulin and other EF-hand proteins to modulate calcineurin activity and subsequent NFAT transcription factor activation. Thus, EFCAB14 operates within the Ca2+?CCaMKII?Ccalcineurin?CNFAT signaling axis, bridging calcium fluctuations to transcriptional responses that govern cell proliferation and apoptosis.
In the SK-HEP-1 cellular context, knockout of EFCAB14 disrupts this calcium-mediated signaling network, potentially altering tumor cell behavior. Given SK-HEP-1’s relevance to hepatocellular carcinoma, this model enables the dissection of calcium-dependent mechanisms underlying liver cancer progression. The loss of EFCAB14 may impair the normal activation of calcineurin and NFAT, thereby affecting expression of genes involved in cell cycle control, survival, and metastasis. This model is particularly suited to examine how calcium dysregulation contributes to hepatocellular carcinoma and related calcium dysregulation disorders, providing a physiologically relevant platform for mechanistic studies.
This knockout cell population supports a wide range of research applications, including functional characterization of EFCAB14, calcium signaling studies, and drug target validation for hepatocellular carcinoma. Researchers can employ representative assays such as Western blotting and RT-qPCR to confirm target disruption and downstream effects, calcium imaging to monitor real-time calcium dynamics, cell proliferation and migration/invasion assays to assess phenotypic changes, and apoptosis assays or RNA-seq to delineate global transcriptional consequences. This product enables robust investigation of EFCAB14-dependent pathways and the development of novel therapeutic strategies. For more information, please contact Ascent Research.
