Robert Hugh Lee

Research Assistant Professor

University of North Carolina at Chapel Hill

United States

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Robert Hugh Lee is a Research Assistant Professor at the University of North Carolina at Chapel Hill. His research areas include hemostasis, platelet function, and thromboembolic disorders, as evidenced by his recent articles on topics such as vascular Ehlers–Danlos syndrome, antiplatelet therapy, and the mechanisms of thrombus formation. His work significantly contributes to the understanding of platelet dynamics and their role in various thrombosis-related conditions.

Articles (12)

Year:

2025

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2025

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2024

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2024

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2024

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2024

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2023

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2022

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2022

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2022

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2022

Year:

2021

Collaborators (9)

Sidney Whiteheart

Professor

University of Kentucky

UNITED STATES

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Woosuk Steve Hur

Research Assistant Professor

University of North Carolina at Chapel Hill

UNITED STATES

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BOJING SHAO

Assistant Member/Head

New York Proton Center

UNITED STATES

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Claire Whyte

University of Aberdeen

UNITED KINGDOM

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Nicholas Smith

University of Washington

UNITED STATES

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Silvio Antoniak

University of North Carolina at Chapel Hill

UNITED STATES

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Stephen R Baker

Research Assistant Professor

Wake Forest University

UNITED STATES

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Tomohiro Kawano

Assistant Professor

Osaka University

JAPAN

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Wolfgang Bergmeier

University of North Carolina

UNITED STATES

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Robert Hugh Lee

Research Interests

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About

Articles (12)

Lack of overt bleeding or platelet dysfunction in a mouse model of vascular Ehlers–Danlos syndrome

Impact of antiplatelet therapy on hemostatic plug formation in the setting of thrombocytopenia

Activated platelets retain and protect most of their factor XIII-A cargo from proteolytic activation and degradation

Utility of thromboelastography with platelet mapping for monitoring platelet transfusion in qualitative platelet disorders

4D intravital imaging studies identify platelets as the predominant cellular procoagulant surface in a mouse hemostasis model

Mice expressing nonpolymerizable fibrinogen have reduced arterial and venous thrombosis with preserved hemostasis

The CalDAG-GEFI/Rap1/αIIbβ3 axis minimally contributes to accelerated platelet clearance in mice with constitutive store-operated calcium entry

Genetic deletion of platelet PAR4 results in reduced thrombosis and impaired hemostatic plug stability

Both G protein–coupled and immunoreceptor tyrosine-based activation motif receptors mediate venous thrombosis in mice

Rasa3 deficiency minimally affects thrombopoiesis but promotes severe thrombocytopenia due to integrin-dependent platelet clearance

Deletion of platelet CLEC-2 decreases GPIbα-mediated integrin αIIbβ3 activation and decreases thrombosis in TTP

Heightened activation of embryonic megakaryocytes causes aneurysms in the developing brain of mice lacking podoplanin

Collaborators (9)

Sidney Whiteheart

Woosuk Steve Hur

BOJING SHAO

Claire Whyte

Nicholas Smith

Silvio Antoniak

Stephen R Baker

Tomohiro Kawano

Wolfgang Bergmeier

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