Research Group Lab Hall
Gilbert C. White, II, MD

Gilbert C. White, II, MD

Emeritus Associate Director, Medical Scientist Training Program; Executive Vice President for Research and Director, Versiti Blood Research Institute; Richard H. and Sara E. Aster Chair for Medical Research, Blood Center of Wisconsin; Professor, Medicine, Biochemistry and Pharmacology and Toxicology; Associate Dean for Research, Medical College of Wisconsin


  • Versiti 230

Contact Information

Research Experience

  • 1-Alkyl-2-acetylglycerophosphocholine Esterase
  • Antigens, Human Platelet
  • Aspirin
  • Bernard-Soulier Syndrome
  • beta-Thromboglobulin
  • Blood Coagulation Disorders
  • Blood Platelet Disorders
  • Blood Platelets
  • Clot Retraction
  • Disintegrins
  • Factor IX
  • HELLP Syndrome

Research Interests

The overall goal of the White lab is to understand the signaling pathways that mediate the hemostatic responses of blood platelets. Understanding these responses at a molecular level permits the development of methods to selectively and precisely manipulate those pathways, thereby controlling vascular diseases like heart attacks and strokes. A current focus is the role of rap1b, a low molecular weight GTP binding protein member of the ras superfamily, which is present in high concentrations in platelets and plays a role in the activation in platelets, including platelet aggregation, the integrin-mediated interaction of one platelet with another to form a platelet hemostatic plug. Rap1b also plays a role in the inhibition of platelets by cyclic AMP. Thus, rap1b appears to be positioned as a unique and critical bi-directional modulator of platelet activation. Using knock-out and transgenic mice combined with proteomic and genetic approaches like yeast two-hybrid screening, we are exploring the pathway(s) by which rap1b and other proteins mediate signals from G-protein coupled receptors such as P2Y12 to integrins like aIIbb3 that mediate platelet aggregation. We are also exploring the pathway(s) that link cyclic AMP and rap1b. Understanding the rap1b-dependent pathways that are involved in mediating platelet responses will provide new ways to control platelet in vascular diseases.