Abstract
Protein Z (PZ) is a vitamin K dependent factor with no enzymatic activity, synthesized mainly by the liver [1]. It acts as an activator of a serpin, the protein Z dependent inhibitor (ZPI), which inhibits factor Xa. In human plasma, there is an excess of ZPI relative to PZ, all the PZ circulates in a complex form with ZPI [2]. A modest prothrombotic phenotype in PZ or ZPI deficient mice [3,4] suggested that PZ and ZPI could play a role in the defense against thrombosis, but in different clinical studies, controversial consequences of PZ or ZPI deficiencies were described [5].
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