Page 1 | Search Results | Blood | American Society of Hematology

1-6 of 6

Sort by

Sort Order Select

Journal Articles

The Kunitz-3 domain of TFPI-α is required for protein S–dependent enhancement of factor Xa inhibition

Matthew Ndonwi, Elodee A. Tuley, George J. Broze, Jr

Blood (2010) 116 (8): 1344–1351.

https://doi.org/10.1182/blood-2009-10-246686

Published: 2010

Journal Articles

Crystal Structure of Von Willebrand Factor (VWF) A1 Domain in Complex with Aptamer ARC1172, An Inhibitor of VWF-Platelet Binding

Ren-Huai Huang, PhD, David Fremont, PhD, Elodee A Tuley, John L Diener, PhD, Robert G Schaub, PhD, J. Evan Sadler, MD, PhD

Blood (2008) 112 (11): 257.

https://doi.org/10.1182/blood.V112.11.257.257

Published: 2008

Journal Articles

Platelet-VWF complexes are preferred substrates of ADAMTS13 under fluid shear stress

Kyuhwan Shim, Patricia J. Anderson, Elodee A. Tuley, Erin Wiswall, J. Evan Sadler

Blood (2008) 111 (2): 651–657.

https://doi.org/10.1182/blood-2007-05-093021

Published: 2008

Journal Articles

A C-Terminal Exosite of von Willebrand Factor Domain A2 Interacts with ADAMTS13 Spacer Domain To Accelerate Substrate Cleavage.

Weiqiang Gao, MD, PhD, Patricia J. Anderson, PhD, Elaine M. Majerus, MD, PhD, Elodee A. Tuley, J. Evan Sadler, MD, PhD

Blood (2006) 108 (11): 1785.

https://doi.org/10.1182/blood.V108.11.1785.1785

Published: 2006

Journal Articles

The C-Terminal α-Helix of von Willebrand Factor Domain A2 Interacts with ADAMTS13 C-Terminal Domains To Regulate Substrate Cleavage.

Weiqiang Gao, MD, PhD, Patricia J. Anderson, Ph.D, Elaine M. Majerus, MD, Ph.D, Elodee A. Tuley, J. Evan Sadler, MD,Ph.D

Blood (2005) 106 (11): 410.

https://doi.org/10.1182/blood.V106.11.410.410

Published: 2005

Journal Articles

Type 1 von Willebrand disease mutation Cys1149Arg causes intracellular retention and degradation of heterodimers: a possible general mechanism for dominant mutations of oligomeric proteins

Imre Bodó, Akira Katsumi, Elodee A. Tuley, Jeroen C. J. Eikenboom, Zhengyu Dong, J. Evan Sadler

Blood (2001) 98 (10): 2973–2979.

https://doi.org/10.1182/blood.V98.10.2973

Published: 2001

NARROW

The Kunitz-3 domain of TFPI-α is required for protein S–dependent enhancement of factor Xa inhibition

Crystal Structure of Von Willebrand Factor (VWF) A1 Domain in Complex with Aptamer ARC1172, An Inhibitor of VWF-Platelet Binding

Platelet-VWF complexes are preferred substrates of ADAMTS13 under fluid shear stress

A C-Terminal Exosite of von Willebrand Factor Domain A2 Interacts with ADAMTS13 Spacer Domain To Accelerate Substrate Cleavage.

The C-Terminal α-Helix of von Willebrand Factor Domain A2 Interacts with ADAMTS13 C-Terminal Domains To Regulate Substrate Cleavage.

Type 1 von Willebrand disease mutation Cys1149Arg causes intracellular retention and degradation of heterodimers: a possible general mechanism for dominant mutations of oligomeric proteins

Email alerts

ASH Publications

American Society of Hematology

The Kunitz-3 domain of TFPI-α is required for protein S–dependent enhancement of factor Xa inhibition

Crystal Structure of Von Willebrand Factor (VWF) A1 Domain in Complex with Aptamer ARC1172, An Inhibitor of VWF-Platelet Binding

Platelet-VWF complexes are preferred substrates of ADAMTS13 under fluid shear stress

A C-Terminal Exosite of von Willebrand Factor Domain A2 Interacts with ADAMTS13 Spacer Domain To Accelerate Substrate Cleavage.

The C-Terminal α-Helix of von Willebrand Factor Domain A2 Interacts with ADAMTS13 C-Terminal Domains To Regulate Substrate Cleavage.

Type 1 von Willebrand disease mutation Cys1149Arg causes intracellular retention and degradation of heterodimers: a possible general mechanism for dominant mutations of oligomeric proteins

Email alerts

ASH Publications

American Society of Hematology

This Feature Is Available To Subscribers Only