The BLVRB Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from A-549 human lung adenocarcinoma cells. This product enables targeted disruption of the BLVRB gene, encoding biliverdin reductase B, a multifunctional enzyme in heme degradation, bilirubin metabolism, and redox homeostasis. The polyclonal format provides a heterogeneous pool of edited cells for robust loss-of-function studies, avoiding artifacts from monoclonal selection. Researchers can use this model to interrogate BLVRB-dependent processes across a representative cell population.
The A-549 cell line was established from a 58-year-old male with lung adenocarcinoma. These adherent epithelial cells retain an alveolar phenotype, serving as a well-characterized model of human lung adenocarcinoma. Widely used in cancer research for oncogenic signaling, drug response, and metastasis studies, their epithelial origin and lung markers make them suitable for investigating alveolar functions and pathways such as oxidative stress and metabolic deregulation.
BLVRB functions as an NADPH-dependent biliverdin reductase, catalyzing the reduction of biliverdin IX?? to the antioxidant bilirubin IX??. It also exhibits flavin reductase activity and possesses intrinsic kinase and transcription factor functions. Operating downstream of HO-1 in heme degradation, it interacts with NADPH, FMN, and biliverdin IX??. BLVRB is regulated by Nrf2 in response to ROS and participates in MAPK/ERK signaling, linking oxidant status to signal transduction. By generating reduced flavins and bilirubin IX??, it contributes to ROS detoxification and NADP+ maintenance, impacting metabolic and redox networks.
In A-549 lung adenocarcinoma cells, BLVRB-mediated redox regulation is critical due to elevated oxidative stress. Disruption of BLVRB helps dissect its role in protecting cancer cells from oxidative damage and supporting proliferative signaling. Given MAPK/ERK pathway involvement in lung cancer, this knockout system reveals how bilirubin metabolism intersects with growth factor signaling. Originating from alveolar epithelium, this model offers insights into pulmonary epithelial biology and response to oxidants, potentially linking BLVRB to lung tumorigenesis and chemoresistance.
This polyclonal knockout product suits a wide range of applications, including western blotting, RT-qPCR, biliverdin reductase activity assays, bilirubin quantification, and ROS detection with DCFDA. Researchers can assess cell viability under oxidative stress, apoptosis via Annexin V/PI flow cytometry, and transcriptomic changes by RNA-seq. These tools enable mechanistic studies of heme catabolism, antioxidant defense, and kinase signaling in lung adenocarcinoma, aiding therapeutic development for oxidative stress-related diseases. For further information, contact Ascent Research.
