DCP antibody

In liver cells, prothrombin precursors are modified by vitamin K(Vit K) -dependent gamma-glutamylcarboxylase to synthesize normal prothrombin, in which all 10 glutamic acid (Glu) residues in the n-terminal domain are converted to gamma-carboxylated glutamic acid residues (Gla). If Vit K is deficient or antagonized, glutamic acid residues fail to fully carboxylate thrombin, abnormal prothrombin (PIVKA-II), also known as des-γ-carboxy-prothrombin (DCP), is formed. Due to the number and location of uncarboxylated glutamic acid residues, abnormal prothrombin will show a diversity of structure and species. It is widely believed that the production of PIVKA-II is mainly related to the decreased activity of gamma-glutacylcarboxylase, the deficiency of Vit K or the dysfunction of metabolic utilization.

Difference between PIVKA-II and Normal prothrombin (N-terminal)