Premium
Vitamin B 12 ‐Binding Protein Abnormality in Subjects without Myeloproliferative Disease: II. THE PRESENCE OF A THIRD VITAMIN B 12 ‐BINDING PROTEIN IN SERUM
Author(s) -
Carmel Ralph
Publication year - 1972
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1972.tb08786.x
Subject(s) - vitamin , vitamin d binding protein , endocrinology , medicine , globulin , vitamin b , binding protein , chemistry , alpha globulin , immunology , biology , biochemistry , gene
Summary. An elevated unsaturated vitamin B 12 binding capacity (UBBC) had been observed in the sera of most subjects with leucocytosis of varying degrees and a few without evident leucocytosis. Although true alpha‐ and beta‐globulin binder increases of varying degree occurred, the increase in UBBC in most subjects was due mainly to a third vitamin B 12 ‐binding protein. In addition, when UBBC fell as leucocytosis subsided, the third binder was no longer detectable. This protein resembles alpha‐globulin binder, or Transcobalamin (TC) I, in molecular weight, antigenic characteristics, and poor mediation of 57 Co B 12 uptake by reticulocytes. It resembles beta‐globulin binder, or TC II, in its behaviour on DEAE‐cellulose batch separation, electrophoretic mobility at pH 8.6, and, as suggested by indirect evidence, probably not carrying endogenous vitamin B 12 . Thus it appears identical to a serum binder previously thought to occur only in polycythaemia vera. It is apparent that the protein is present in large amounts in a variety of conditions involving leucocytosis, and possibly occurs in normal serum in small quantities also. It is possible that the binder may be an altered form of TCI. The reason for the predominance of TCI in some conditions involving granulocytic proliferation, and this binder in others, is unknown.