Anti-Transferrin antibody - Serum Loading Control

Supplementary information

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

Transferrin also known as serotransferrin or siderophilin is a glycoprotein with a mass of approximately 80 kDa. It is primarily synthesized in the liver and subsequently secreted into the bloodstream. Transferrin has an important role in iron transport and maintains iron homeostasis by binding and delivering iron to various tissues throughout the body. It can bind two ferric ions (Fe3+) in association with an anion usually bicarbonate. In biological fluids transferrin exists in serum plasma and other extracellular fluids.

Biological function summary

Transferrin facilitates the transportation of iron ions. It delivers iron to cells by binding to transferrin receptors on cell surfaces forming a complex that gets internalized via receptor-mediated endocytosis. Inside the endosomes acidic conditions cause iron to release from transferrin enabling its utilization in cellular processes like DNA synthesis and electron transport. Transferrin itself acts independently and does not form part of a larger protein complex. Variants of transferrin include mouse transferrin bovine transferrin and biotinylated transferrin each with similar function across different species.

Pathways

Transferrin operates centrally in iron metabolism and homeostasis pathways. It functions in coordination with the transferrin receptor 1 (TfR1) which facilitates cellular uptake of the transferrin-iron complex. Additionally transferrin plays a role in the hepcidin regulatory pathway. Hepcidin modulates iron homeostasis by decreasing iron absorption in the intestine and controlling iron release from macrophages and hepatocytes. Transferrin's ability to bind iron connects it to other iron-containing proteins such as ferritin which stores excess iron in cells.

Several iron-related conditions can impact transferrin function including anemia and hemochromatosis. Anemia often occurs when there is insufficient iron delivery leading to inadequate hemoglobin synthesis and reduced oxygen transport. Aberrant transferrin receptor activity affects iron uptake in such conditions. Hemochromatosis characterized by iron overload can occur due to mutations in genes like HFE leading to changes in hepcidin regulation and increased intestinal iron absorption. Transferrin levels and saturation are clinical indicators used to assess iron status in such diseases.