PE Anti-Glucose Transporter GLUT1 antibody [EPR3915]

Supplementary info

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

Activity summary

The Glucose Transporter GLUT1 also known as SLC2A1 is an important protein responsible for the transport of glucose across cell membranes. The GLUT1 transporter has a molecular weight of approximately 55 kDa. This protein is highly expressed in erythrocytes endothelial cells lining blood vessels and in the blood-brain barrier. Its primary role is to facilitate the basal glucose uptake necessary for cellular metabolism particularly in tissues where glucose is a critical energy source.

Biological function summary

This glucose transporter plays a significant role in maintaining glucose homeostasis in the human body. GLUT1 functions independently and not as part of a complex. It ensures that glucose is available to cells with high metabolic demands including the brain and red blood cells where it remains important for survival and function. Its expression level can be influenced by various factors including hypoxia and insulin.

Pathways

GLUT1 is involved in the glycolysis and hypoxia-related pathways. It supports the glycolytic pathway by ensuring a sufficient supply of glucose to the cells which is then metabolized to produce ATP. Additionally during hypoxic conditions GLUT1 expression can increase aligning with proteins like HIF-1α which helps cells adapt by modifying their metabolism. This coordinated regulation permits cells to adjust their energy systems according to the oxygen availability.

Associated diseases and disorders

GLUT1 is implicated in glucose transporter type 1 deficiency syndrome (GLUT1 DS) and various forms of cancer. GLUT1 DS results from inadequate glucose transport into the brain presenting neurological symptoms due to energy deficiency. In cancer overexpression of GLUT1 links to increased glucose uptake and tumor growth a condition known to involve proteins like hexokinase. These associations underline GLUT1's contribution to both genetic defects and metabolic shifts in cancerous tissues.