Abstract: The presently disclosed subject matter provides a mechanism in which DVTs form when reduced muscular activity results in loss of oscillatory shear-dependent transcriptional and ant-thrombotic phenotypes in peri-valvular venous endothelial cells. Endothelial cells surrounding the venous valve, where DVTs originate, experience oscillatory shear forces in response to muscular activity. Peri-valvular venous endothelial cells express high levels of FOXC2 and PROX1, transcription factors known to be activated by oscillatory shear stress, exhibit an anti-thrombotic phenotype characterized by low levels of the procoagulant proteins von Willebrands Factor (vWF), P-selectin and intercellular adhesion molecule 1 (ICAM1), high levels of the anticoagulant proteins thrombomodulin (THBD), endothelial protein C receptor (EPCR) and tissue factor pathway inhibitor (TFPI), and resistance to thrombin-induced clot formation.

Abstract: Disclosed herein are methods for producing compounds (such as 3,4-dihydroxybenzoate, catechol, cis,cis-muconate, or ?-carboxy-cis,cis-muconic acid) utilizing biosynthetic pathways in prokaryotic organisms expressing one or more heterologous genes. In some embodiments, the method includes expressing a heterologous asbF gene (for example, a gene having dehydroshikimate dehydratase activity) in a prokaryotic cell under conditions sufficient to produce the one or more compounds and purifying the compound. In additional embodiments, the method further includes expressing one or more of a heterologous 3,4-DHB decarboxylase gene, a heterologous catechol 1,2-dioxygenase gene, and a heterologous 3,4-DHB dioxygenase gene in the prokaryotic cell and purifying the compound.

Abstract: The present invention relates to compounds and methods for inhibiting cancer metastasis. In an embodiment, the compound of the present invention contains the sulfatide binding region of the terminal phosphotyrosine binding domain (N-PTB) of Disabled-2 (Dab2).

Abstract: Disclosed herein are methods for producing compounds (such as 3,4-dihydroxybenzoate, catechol, cis,cis-muconate, or ?-carboxy-cis,cis-muconic acid) utilizing biosynthetic pathways in prokaryotic organisms expressing one or more heterologous genes. In some embodiments, the method includes expressing a heterologous asbF gene (for example, a gene having dehydroshikimate dehydratase activity) in a prokaryotic cell under conditions sufficient to produce the one or more compounds and purifying the compound. In additional embodiments, the method further includes expressing one or more of a heterologous 3,4-DHB decarboxylase gene, a heterologous catechol 1,2-dioxygenase gene, and a heterologous 3,4-DHB dioxygenase gene in the prokaryotic cell and purifying the compound.

Abstract: The present invention relates to compounds and methods for inhibiting platelet aggregation. In an embodiment, the compound of the present invention contains the sulfatide binding region of the N-terminal phosphotyrosine binding domain (N-PTB) of Disabled-2 (Dab2).