Anti-HMGCR (phospho S872) antibody

Supplementary info

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

Activity summary

HMG-CoA reductase also known as HMGCR plays an important role in cholesterol biosynthesis. This enzyme catalyzes the conversion of HMG-CoA (3-hydroxy-3-methyl-glutaryl-coenzyme A) to mevalonate a critical step in the isoprenoid synthesis pathway. HMGCR is a membrane-bound enzyme located primarily in the liver on the endoplasmic reticulum. The enzyme has a molecular mass of approximately 97 kDa. Due to its central role in cholesterol metabolism HMGCR has become a primary target for statins such as pravastatin and simvastatin.

Biological function summary

HMGCR reduces HMG-CoA to mevalonate an important precursor for several important biomolecules including cholesterol. It exists as part of a complex regulatory system impacted by intracellular cholesterol levels. The activity of HMGCR is tightly controlled through feedback inhibition and post-translational modifications. The enzyme interacts with other proteins in the endoplasmic reticulum as part of the cholesterol homeostatic mechanism in cells expressing it including hepatocytes.

Pathways

HMGCR is an essential component of the mevalonate pathway which is important for the synthesis of sterols and non-sterol isoprenoids. This pathway also intersects with the biosynthesis of ubiquinone and dolichol. The regulation of cholesterol synthesis involves the coordinated activity of HMG-CoA reductase and LDL receptor proteins. Their interplay ensures a balanced cholesterol level and integrates with the response to cellular demands and dietary intake.

Associated diseases and disorders

HMGCR is strongly linked to cardiovascular diseases due to its influential role in cholesterol synthesis. Inhibitors like pravastatin and simvastatin effectively lower blood cholesterol levels and reduce the risk of coronary artery disease by targeting HMGCR. The Statins also have potential associations with muscular disorders because of shared pathways involving proteins such as SREBP (sterol regulatory element-binding proteins) which regulate the transcription of genes involved in lipid metabolism.