APC Anti-CYP11A1 antibody [EPR24868-86]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

CYP11A1 also called cytochrome P450scc is an important enzyme that catalyzes the first step in steroid hormone biosynthesis. This enzyme has a molecular weight of approximately 60 kDa. It is primarily located in the mitochondria of steroidogenic tissues such as the adrenal cortex testes and ovaries. CYP11A1 converts cholesterol into pregnenolone a precursor for all steroid hormones. Its gene expression is tightly regulated by trophic hormones which play an important role in modulating steroid production.

Biological function summary

CYP11A1 is a member of the cytochrome P450 superfamily a large group of enzymes known for their role in oxidation and metabolism. It exists in the mitochondrial electron transport chain working closely with proteins such as ferredoxin and ferredoxin reductase. These interactions facilitate the conversion of cholesterol to pregnenolone. Through these biochemical activities CYP11A1 controls the synthesis rate of steroid hormones influencing various physiological functions including metabolism immune response and reproductive system dynamics.

Pathways

CYP11A1 operates within the steroidogenesis pathway which is essential for the synthesis of steroid hormones like cortisol and aldosterone. It directly interacts with StAR protein which transports cholesterol into mitochondria initiating the steroidogenesis process. Moreover CYP11A1 fits into the pregnenolone biosynthesis pathway showing functional connectivity with other cytochrome P450 enzymes like CYP17A1. These interconnected pathways highlight the role of CYP11A1 as a vital catalyst in hormone synthesis affecting both endocrine and metabolic pathways.

Associated diseases and disorders

CYP11A1 mutations or expression abnormalities have associations with conditions such as congenital adrenal hyperplasia (CAH) and primary adrenal insufficiency. CAH arises from enzyme deficiencies in the steroidogenesis pathway and changes in CYP11A1 activity can exacerbate the disorder by altering cortisol and aldosterone synthesis. Additionally the enzyme’s link with StAR protein suggests a possible connection to lipoid congenital adrenal hyperplasia where defects in cholesterol transport may disrupt steroid production. Understanding these relationships helps in exploring therapeutic targets for steroid-related diseases.