Abstract

von Willebrand Factor (vWF) is a multimeric protein that mediates platelet adhesion to exposed subendothelium at sites of vascular injury under conditions of high flow/shear. The A1 domain of vWF (vWF-A1) forms the principal binding site for platelet glycoprotein Ib (GpIb), an interaction that is tightly regulated. We report here the crystal structure of the vWF-A1 domain at 2.3-A resolution. As expected, the overall fold is similar to that of the vWF-A3 and integrin I domains. However, the structure also contains N- and C-terminal arms that wrap across the lower surface of the domain. Unlike the integrin I domains, vWF-A1 does not contain a metal ion-dependent adhesion site motif. Analysis of the available mutagenesis data suggests that the activator botrocetin binds to the right-hand face of the domain containing helices alpha5 and alpha6. Possible binding sites for GpIb are the front and upper surfaces of the domain. Natural mutations that lead to constitutive GpIb binding (von Willebrand type IIb disease) cluster in a different site, at the interface between the lower surface and the terminal arms, suggesting that they disrupt a regulatory region rather than forming part of the primary GpIb binding site. A possible pathway for propagating structural changes from the regulatory region to the ligand-binding surface is discussed.

Highlights

  • Von Willebrand Factor1 is a multimeric protein that mediates platelet adhesion to exposed subendothelium at sites of vascular injury [1]

  • A reduction in the plasma concentration of von Willebrand Factor (vWF) or mutations that impair binding, activation, or assembly of vWF multimers cause von Willebrand disease, a common bleeding disorder characterized by decreased platelet adhesion and mucocutaneous bleeding [2]

  • In 1995, we reported the crystal structure of the first family member, the I domain of the leukocyte integrin ␣M␤2 [8], and the crystal structures of several A domains have been solved (9 –12)

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Summary

Introduction

Von Willebrand Factor (vWF) is a multimeric protein that mediates platelet adhesion to exposed subendothelium at sites of vascular injury [1]. Mediated by sequences within the first (A1 domain) and third (A3 domain) A type repeats of vWF. The vWF-A3 domain contains the principal site for binding the fibrillar collagens types I and III [5, 6]. Initially noted in the primary sequence of vWF, the A domain has been subsequently discovered in a large number of cell matrix-associated or adhesive proteins and receptors [7]. The integrin I domains contain a metal ion-dependent adhesion site (MIDAS) on the upper face of the domain that is an important element of ligand binding [8, 13,14,15]. The vWF-A3 domain does not bind metal and does not require metal for binding to collagen [10]

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