4X1D, 1A8E, 1A8F, 1B3E, 1BP5, 1BTJ, 1D3K, 1D4N, 1DTG, 1FQE, 1FQF, 1JQF, 1N7W, 1N7X, 1N84, 1OQG, 1OQH, 1RYO, 1SUV, 2HAU, 2HAV, 2O7U, 2O84, 3FGS, 3QYT, 3S9L, 3S9M, 3S9N, 3SKP, 3V83, 3V89, 3V8X, 3VE1, 4H0W, 4X1B, 5DYH701822041ENSG00000091513ENSMUSG00000032554P02787Q921I1NM_001063NM_001354704NM_001354703NM_133977NP_001054NP_001341633NP_001341632NP_598738Transferrins are glycoproteins found in vertebrates which bind and consequently mediate the transport of iron (Fe) through blood plasma.

Transferrin has a molecular weight of around 80 kDa and contains two specific high-affinity Fe(III) binding sites.

[11] Iron release rate is dependent on several factors including pH levels, interactions between lobes, temperature, salt, and chelator.

[14] The receptor with its ligand bound transferrin is then transported through the endocytic cycle back to the cell surface, ready for another round of iron uptake.

A major source of transferrin secretion in the brain is the choroid plexus in the ventricular system.

[15] The main role of transferrin is to deliver iron from absorption centers in the duodenum and white blood cell macrophages to all tissues.

Transferrin plays a key role in areas where erythropoiesis and active cell division occur.

This finding helps in the early diagnosis of Hereditary hemochromatosis, especially while serum ferritin still remains low.

This explains why ferritin levels remain relative low in Hereditary hemochromatosis, while transferrin saturation is high.

[16] Many drugs are hindered when providing treatment when crossing the blood-brain barrier yielding poor uptake into areas of the brain.

[25] Due to this functionality, it is theorized that nanoparticles acting as drug carriers bound to transferrin glycoproteins can penetrate the blood-brain barrier allowing these substances to reach the diseased cells in the brain.

[27] Carbohydrate deficient transferrin increases in the blood with heavy ethanol consumption and can be monitored through laboratory testing.

In nephrotic syndrome, urinary loss of transferrin, along with other serum proteins such as thyroxine-binding globulin, gammaglobulin, and anti-thrombin III, can manifest as iron-resistant microcytic anemia.