CYP7A1 Recombinant Mouse mAb (S-M0026)

CYP7A1 (cholesterol 7α-hydroxylase), a member of the cytochrome P450 superfamily, is highly expressed primarily in the liver. As the rate-limiting enzyme of the classical pathway of bile acid synthesis, it catalyzes the conversion of cholesterol into 7α-hydroxycholesterol, which is the critical first step in generating primary bile acids (cholic acid and chenodeoxycholic acid). This protein plays an irreplaceable physiological role in maintaining cholesterol homeostasis, facilitating lipid digestion and absorption, and eliminating excess cholesterol. Its expression is finely regulated by bile acids, hormones, and circadian rhythms: high concentrations of bile acids inhibit CYP7A1 transcription by activating the farnesoid X receptor (FXR), forming a negative feedback loop, whereas insulin upregulates its expression to promote the conversion of cholesterol into bile acids. Dysfunction of CYP7A1 is closely associated with various metabolic diseases—reduced activity can lead to hypercholesterolemia and gallstone formation, while excessive activity may accelerate bile acid loss, triggering pathological conditions such as nonalcoholic steatohepatitis or diarrhea.