The BLVRB Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal cell population engineered to disrupt the BLVRB gene in the SK-HEP-1 human liver adenocarcinoma cell line. This product provides a heterogeneous pool of cells with diverse loss-of-function mutations, enabling the study of BLVRB deficiency in a population context without the need for monoclonal selection.
The host SK-HEP-1 cell line, established from the ascites fluid of a patient with liver adenocarcinoma, exhibits endothelial-like characteristics and is widely used as a model for hepatocellular carcinoma and hepatic sinusoidal endothelium. This background is particularly relevant for investigating BLVRB function in liver-specific oxidative stress responses and cancer signaling.
BLVRB encodes biliverdin reductase B, which catalyzes the NADH/NADPH-dependent reduction of biliverdin-IX-alpha to the potent antioxidant bilirubin-IX-alpha. Additionally, BLVRB functions as a dual-specificity kinase that phosphorylates and activates AKT and ERK, and as a transcription factor regulating antioxidant genes such as GCLM and thioredoxin. Its expression is induced by NRF2 and HIF-1?? in response to oxidative stress and hypoxia, and it interacts with heme oxygenase-1 (HO-1), biliverdin reductase A (BLVRA), and biliverdin-IX-alpha. These signals converge on downstream effectors including phosphorylated AKT, phosphorylated ERK, and NF-??B, integrating heme degradation with cell survival and redox homeostasis.
In SK-HEP-1 hepatocellular carcinoma cells, disruption of BLVRB impairs bilirubin-mediated antioxidant defense and attenuates AKT/ERK-dependent prosurvival signaling. This knockout model is instrumental for dissecting the contribution of BLVRB to oncogenic transformation, resistance to oxidative damage, and adaptation to hypoxia, offering insights into the molecular interplay between metabolism and cancer progression.
Researchers can employ this polyclonal knockout population to investigate heme degradation and bilirubin metabolism, explore the kinase and transcription factor roles of BLVRB, and screen for compounds that modulate BLVRB-related pathways. Compatible assays include western blotting for BLVRB and phosphorylated AKT/ERK, RT-qPCR, biliverdin reductase activity assays, intracellular bilirubin fluorometry, ROS detection with DCF-DA, MTT or Annexin V assays, co-immunoprecipitation of BLVRB with AKT, and NF-??B reporter assays. For further information, please contact Ascent Research.
