Salk Institute

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A Novel Animal Model for Studying Anticoagulants: Protein S Deficient Mice

Inventors: Tal Burstyn-Cohen, and Greg Lemke
Potential Uses: Drug discovery, stroke, thrombosis, lupus and autoimmunity

Embryonic lethal coagulopathy and vascular dysgenesis in mice lacking Protein S

Lethal embryonic coagulopathy in Protein S deficient mice. Wild-type (A, C) and Protein S knock out (Pros1-/-) littermates (B, D).  Principal superficial blood vessels that are readily visible in WT (A, arrowheads; are not visible in Pros1-/- littermates (Pros1-/- embryos present with macroscopic thrombi (B, asterisks). (C, D) 300 micrometer coronal brain sections of perfused WT and Pros1-/- embryos, respectively. Perfusion of WT brain yields clear tissue (C) but intravascular thrombi render vessels perfusion- resistant in Pros1-/- brain tissue, and hemorrhages are prominent (D).

Protein S (ProS) is a blood anticoagulant, and ProS deficiencies are associated with venous thrombosis, stroke, and autoimmunity. These associations notwithstanding, the relative risk that reduced ProS expression confers in different disease settings has been difficult to assess without an animal model. This invention provides the first animal model for Protein S deficiency, and provides a novel model for studying the aforementioned diseases, as well as anticoagulants.

ProS is a plasma glycoprotein that acts as a critical negative regulator of blood coagulation. It functions as an essential cofactor for activated Protein C in the degradation of coagulation factors FVa and FVIIIa, and thus operates at a central node in the coagulation cascade. The physiological importance of ProS is dramatically demonstrated by the catastrophic purpura fulminans that develops in the very rare human newborns documented to be homozygous for ProS mutations. Individuals with less severe ProS deficiencies due to heterozygous mutations or polymorphisms, of which more than 200 forms have been documented, are at elevated risk for deep vein thrombosis and other life threatening thrombotic events. This Invention provides a new tool for studying these diseases and developing therapeutic treatments.

Salk No: S08022
Patent Status: U.S. Patent Application submitted March 1, 2009
Publications: Burstyn-Cohen, Heeb, and Lemke. Lack of Protein S in mice causes embryonic lethal coagulopathy and vascular dysgenesis. J Clinical Investigation (2009)
License Terms: Exclusive, partially exclusive, nonexclusive license negotiable
Contact: Michelle Booden, Ph.D., Director of Licensing, 858.453.4100 x1612, mbooden@salk.edu

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