The ITPRIPL2 Knockout SK-HEP-1 Polyclonal Cells provide a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population in which the ITPRIPL2 gene has been disrupted in the SK-HEP-1 host cell line. This product, generated through CRISPR/Cas9-mediated gene disruption, yields a heterogeneous mixture of edited cells, enabling loss-of-function studies without clonal selection artifacts. The polyclonal format preserves the genetic diversity of the edited population, which can be advantageous for capturing a range of knockout efficiencies and minimizing clone-specific biases in downstream functional assays. Researchers can employ this model to interrogate the role of ITPRIPL2 in cellular processes using standard cell culture techniques and molecular readouts.
SK-HEP-1 is a human hepatic adenocarcinoma epithelial cell line originally derived from the ascites of a patient with liver adenocarcinoma. This cell line retains many characteristics of hepatocellular carcinoma, including an epithelial morphology and the expression of hepatic markers, making it a widely used in vitro model for liver cancer biology. SK-HEP-1 cells are frequently employed in studies of tumor cell proliferation, migration, apoptosis, and drug response, providing a physiologically relevant context for investigating the molecular mechanisms underlying hepatocellular carcinoma. Their derivation from a metastatic site (ascites) further renders them valuable for research into the invasive and metastatic properties of liver cancer.
The ITPRIPL2 gene encodes a modulator of inositol 1,4,5-trisphosphate receptor (ITPR) activity, which governs intracellular calcium release from the endoplasmic reticulum. ITPRIPL2 interacts directly with ITPR1, ITPR2, and ITPR3 and the calcium-binding protein calmodulin (CALM) to regulate calcium flux. Activation of upstream signaling via G protein-coupled receptors (GPCRs) and phospholipase C (PLC) generates IP3, which binds to ITPRs; ITPRIPL2 fine-tunes this process. Downstream, cytosolic calcium elevations activate calcineurin?NFAT and calcium/calmodulin-dependent protein kinase II (CAMKII) pathways. Knockout of ITPRIPL2 disrupts this regulatory node, altering calcium homeostasis and impairing calcium-dependent transcriptional and post?translational signaling cascades.
In the hepatocellular carcinoma context of SK-HEP-1 cells, ITPRIPL2 knockout provides a system to dissect the contribution of ITPR-mediated calcium signaling to liver cancer pathology. Dysregulated calcium signaling is implicated in tumor progression, evasion of apoptosis, autophagy, and endoplasmic reticulum stress responses??all of which are relevant to hepatocellular carcinoma. By ablating ITPRIPL2 expression, this model enables the analysis of phenotypic changes in proliferation, survival, and stress adaptation that may depend on calcium dynamics. Moreover, because SK-HEP-1 cells respond to calcium-mobilizing stimuli, the knockout cells can be used to study how ITPRIPL2 modulates oncogenic signaling networks in a disease-relevant cellular background.
Typical applications of this polyclonal knockout product include functional characterization of ITPRIPL2 in calcium signaling, apoptosis, and autophagy; validation of ITPRIPL2 as a potential drug target in liver cancer; and mechanistic studies of endoplasmic reticulum stress. Experimental approaches may involve calcium imaging with fluorescent indicators, quantitative RT?qPCR and Western blotting to monitor ITPRIPL2 and downstream effectors (e.g., NFAT, CAMKII), apoptosis assays using Annexin V/PI staining, cell proliferation analyses, and co?immunoprecipitation of ITPRIPL2 with ITPR isoforms. These cells are suitable for use in both basic research and translational oncology programs. For further details, please contact Ascent Research.
