Abstract
The role of protein Z (PZ) in the etiology of human disorders is unclear. A number of PZ gene variants, sporadic or polymorphic, have been observed in patients with thrombosis or fetal losses, all of them included in the serine protease domain. We previously showed that sporadic mutations within the PZ exon 8 are associated with a ~6-fold higher risk of fetal loss. Crystal structures of PZ in complex with the PZ-dependent inhibitor (PZI) have been recently obtained. A structural investigation of the serine protease PZ domain, aiming at finding common traits across disease-linked mutations, has been undertaken.
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