The cellular function of SCAP in metabolic signaling.

Sterol regulatory element binding protein (SREBP) cleavage activating protein (SCAP) is a key regulator of SREBP maturation. SCAP induces translocation of SREBP from the endoplasmic reticulum to the Golgi apparatus, allowing it to regulate cellular triglyceride and cholesterol levels. Previous studies have shown that suppression of SREBP activation in SCAP conditional knockout mice reduced the accumulation of intracellular triglycerides, which eventually causes the development of metabolic diseases such as atherosclerosis, diabetes, hepatic steatosis, and insulin resistance. However, despite the significance of SCAP as a regulator of SREBP, its function has not been thoroughly discussed. In this review, we have summarized the function of SCAP and its regulatory proteins. Furthermore, we discuss recent studies regarding SCAP as a possible therapeutic target for hypertriglyceridemia and hyperlipidemia. The complex cellular functions of a membrane protein that influences fat and cholesterol levels have been reviewed by researchers in South Korea. The main role of this protein, SCAP, is to move certain transcription factors between organelles within cells, allowing them to regulate the synthesis of triglycerides (fat molecules) and cholesterol. Seung-Soon Im and co-workers at Keimyung University School of Medicine in Daegu reviewed studies of the numerous signalling pathways that influence SCAP activity, and of insulin-induced genes that bind to SCAP and inhibit its function. Genetic studies have shown that blocking SCAP in mice can reduce the development of diabetes, fatty liver disease and atherosclerosis. Several drugs for these metabolic conditions have been shown to indirectly inhibit SCAP activity, and therefore drugs that directly target SCAP should be a focus of future research.