David T. Berg

TL;DR: It is shown that activated protein C (APC) formation is reduced in diabetic mice and causally linked to nephropathy, and a new pathway is established, in which hyperglycemia impairs endothelial thrombomodulin-dependent APC formation.

TL;DR: It is demonstrated that both the γ-carboxyglutamate and glycosyl contents affect the functional activities of rHPC, and the critical dependence of full γ -carboxylation on the function of this protein is demonstrated.

TL;DR: It is suggested that activated protein C can suppress LPS-induced ARF by modulating factors involved in vascular inflammation, including downregulation of renal iNOS and ANG II systems.

TL;DR: It is suggested that soluble thrombomodulin may have therapeutic potential for ischemic AKI after it was determined that the protective effects of sTM were independent of its ability to generate activated protein C.

TL;DR: A vector for the expression of recombinant human protein C (rHPC) was constructed using a hybrid promoter that could be activated in trans by the early region 1A (E1A) proteins of adenovirus.