Human CYP11B1 Stable Cell Line - V79

The CYP11B1 gene, located on chromosome 8 q24.3, encodes steroid 11β-hydroxylase, a key member of the cytochrome P450 superfamily. This mitochondrial enzyme is primarily located in the adrenal cortex, particularly the zona fasciculata and zona reticularis, and is a cornerstone of glucocorticoid biosynthesis. Its main catalytic function is the conversion of 11-deoxycortisol to cortisol, the primary glucocorticoid hormone used in the body to maintain metabolic homeostasis, regulate inflammatory responses, and mediate physiological adaptations to stress. Furthermore, CYP11B1 promotes the hydroxylation of 11-deoxycorticosterone to corticosterone. The transcription and activity of this gene are tightly regulated by adrenocorticotropic hormone (ACTH) via the cyclic adenosine monophosphate (cAMP) signaling pathway. Mutations in the CYP11B1 gene have significant clinical implications because they lead to 11β-hydroxylase deficiency, the second most common cause of congenital adrenal hyperplasia (CAH).

The V79 stable human CYP11B1 cell line is a specially designed recombinant cell model designed to provide a high-fidelity platform for studying the activity and inhibition of human 11β-hydroxylase. By stably transfecting these cells with human CYP11B1 cDNA and the essential mitochondrial redox chaperones adrenocortical feroxin (ADX) and adrenocortical feroxin reductase (ADR), a functional human steroid production system can be reconstructed in an easily maintained in vitro environment. This product has wide applications in the pharmaceutical industry for high-throughput screening of selective inhibitors, which is crucial for the treatment of endocrine disorders such as Cushing''s syndrome and various forms of hypercortisolism. In addition to drug discovery, the V79-CYP11B1 stable cell line also plays an important role in environmental toxicology and safety assessments, serving as a reliable model for detecting endocrine-disrupting chemicals that may interfere with adrenal steroid metabolism.