Computational analysis of the Factor V Leiden mutation and binding differences with Activated Protein C

Willow C. Reese
Dr. Bill R. Miller (A.T. Still University) and Dr. R. Drew Sieg, Faculty Mentors

Factor V Leiden is a blood disorder characterized by excessive clotting caused by a point mutation in the gene coding for residue 506R of the Factor V protein (FacV). FacV Leiden is the leading cause of inherited thrombophilia, affecting 5% of caucasian people and 1 in 50 people of African or Hispanic descent. This excessive clotting is due to an inability of the mutated FacV protein to bind with Activated Protein C (APC) and Protein S (PS), regulatory proteins that bind to the FacV protein, deactivating it and preventing initiation of the coagulation cascade. Through computational methods, such as HADDOCK docking and Amber Molecular Dynamics, this project seeks to characterize the binding between FacV and APC to better understand the specific chemistry preventing FacV deactivation. This work will lay the foundations of future research in pharmaceutical development, allowing for different compounds to be identified to treat or cure this disorder.

 

Keywords: Factor V Leiden, Coagulation Cascade, Computational, Biochemistry, Medicine, Blood Clots, Molecular Dynamics, Protein-Protein Docking

Topic(s):Biochemistry and Molecular Biology
Chemistry
Biology

Presentation Type: Oral Presentation

Session: TBA
Location: TBA
Time: TBA