Transcobalamin III

B2. Burger, R. L., Mehlman, C. S., and Allen, R. H., Human plasma R-type vitamin B12 binding proteins. I. Isolation and characterisation of transcobalamin I, transcobalamin III and the normal granulocyte vitamin B12 binding protein. J. Biol. Chem. 250, 7700-7706 (1975). 

Scott, J. M., Bloomfield, F. J., Stebbins, R., and Herbert, V., Studies on derivation of transcobalamin III from granulocytes Enhancement by lithium and elimination by fluoride of in vitro increments in vitamin B12-binding capacity. /. Clin. Invest. 53, 28-239 (1974). 

There is a third plasma vitamin B12 binding protein, transcobalamin III, which is rapidly cleared by the liver, with a plasma half-life of the order of 5 minutes. This seems to provide a mechanism for returning vitamin B12 and its metabolites from peripheral tissues to the liver, as well as for clearance of other corrinoids without vitamin activity, which may arise either from foods or the products of intestinal bacterial action and be absorbed passively from the lower gut. These corrinoids are then secreted into the bile, bound to cobalophUins. 

Birn, H., Willnow, T. E., Nielsen, R., Norden, A. G., Bonsch, C., Moestrup, S. K., Nexo, E., Christensen, E. I. 2002. Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). Am J Physiol Renal Physiol, 282, F408-16. Burger, R. L., Schneider, R. J., Mehlman, C. S., Allen, R. H. 1975. Human plasma R-type vitamin B 12-binding proteins. II. The role of transcobalamin I, transcobalamin III, and the normal granulocyte vitamin B 12-binding protein in the plasma transport of vitamin B12.J Biol Chem, 250, 7707-13. 

There is a considerable enterohepatic circulation of vitamin B - Vitamin B and its metabolites (some of which are biologically inactive) are transferred from peripheral tissues to the liver bound to transcobalamin III. They are then secreted into the bile, bound to cobalophilins 3-8 Ig (2.25-6 nmol) of vitamin B may be secreted in the... 

Transcobalamin I (R binder) Transcobalamin II Transcobalamin III (R binder) Milk vitamin-Bi2-binding protein... 

Other plasma vitamin B 2 proteins, transcobalamines I and III, appear to have primarily a storage function and only a lesser role in transport. 

Once absorbed, vitamin B12 is transported to the various cells of the body bound to a family of specialized glycoproteins, transcobalamin I, II, and III. Excess vitamin B12 is transported to the liver for storage. 

Approximately 90% of the unsaturated vitamin B12 binding capacity of sonicates of peripheral blood granulocytes appears to be TC III, while the remainder is TC I (S6). Granulocytes have not been found to contain TC II. Studies on the delivery of vitamin B12 to human lymphocytes by TC I, TC II, and TC III have shown that in lymphocyte cultures the uptake of [57Co]B12 from its complex with TC II was substantially higher than from complexes with other binders. It was concluded from these experiments that TC III, like TC I, did not promote uptake of vitamin B12 by human hemopoietic cells and that these two transcobalamins appear to be storage proteins (M2). 

D2. Daiger, S. P., Labone, M. L., Parsons, M., Wang, L., andCavalli-Sforza, L. L., Detection of genetic variation with radioactive ligands. III. Genetic polymorphism of transcobalamin II in human plasma. Am. J. Hum. Genet. 30, 202-214 (1978). 

The serum cobalophilins, transcobalamin I and III (TCI and TCIII), are immunologically identical and may differ only in their carbohydrate content. TCI moves as an a ] -globulin in standard serum protein electrophoresis, while TCIII moves as an a2-globuIin owing to its lower sialic acid content. Plasma TCIII... 

Once absorbed, vitamin Bjj binds to transcobalamin II, a plasma /5-globulin, for transport to tissues. Two other transcobalamins (I and III) also are present in plasma their concentrations are related to the rate of turnover of granulocytes. They may represent intracellular storage proteins that... 

FIGURE 53-8 The absorption and distribution of vitamin Deficiency of vitamin can result from a congenital or acquired defect in any one of the following (1) inadequate dietary supply (2) inadequate secretion of intrinsic factor (classical pernicious anemia) (3) ileal disease (4) congenital absence of transcobalamin II (Tell) or (5) rapid depletion of hepatic stores by interference with reabsorption of vitamin excreted in bile. The utility of measurements of the concentration of vitamin B 2 tn plasma to estimate supply available to tissues can be compromised by liver disease and (6) the appearance of abnormal amounts of transcobalamins I and III (Tcl and III) in plasma. Finally, the formation of methylcobalamin requires (7) normal transport into cells and an adequate supply of folic acid as CH H PteGlu. ... 

Allen, R. H., and Majems, P. W., 1972b, Isolation ofvitamm B12-binding proteins using affinity chromatography III. Purification and properties of human plasma transcobalamin II. J. Biol Chem. 242 7709-7717. 

Bi2 is present in holoTC, the remaining eobalamin is bound to transcobalamin (TC) I and III. Figure 28.1 summarizes this complex process. 

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