World's Best Scientists 2026 revealed!

D-Index & Metrics

Biology and Biochemistry

D-Index
42
Citations
12247
World Ranking
19443
National Ranking
7930

Overview

Naomi L. Esmon is affiliated with the Oklahoma Medical Research Foundation in the United States. Their research primarily focuses on the field of medicine, with significant contributions in hematology, genetics, and immunology. The main areas of study include hemophilia treatment and research, blood coagulation and thrombosis mechanisms, coagulation-related pathways involving bradykinin, polyphosphates, and angioedema, as well as the roles of neutrophils, myeloperoxidase, and oxidative mechanisms. They have also worked on platelet disorders and myeloproliferative neoplasms concerning diagnosis and treatment.

As an active contributor to scientific literature, Naomi L. Esmon has published research in several prominent venues, with frequent publications in Blood and Blood Advances. Their recent papers include:

  • Blocking human protein C anticoagulant activity improves clotting defects of hemophilia mice expressing human protein C, 2022, Blood Advances
  • Safety and efficacy of an anti-human APC antibody for prophylaxis of congenital factor deficiencies in preclinical models, 2023, Blood
  • EPCR Signaling Controls the Activity of Hematopoietic Stem Cells Independent of Coagulation Regulation, 2021, Blood

Collaborative work is a consistent aspect of their research, with frequent co-authorship alongside other scientists including Miao Jiang, Fei Yang, Yizhi Jiang, Lu Cheng, and Jingjing Han. Each of these collaborators has worked with Naomi L. Esmon on multiple publications, indicating ongoing research partnerships.

Their work spans a complex range of topics within hematology and related biomedical fields, emphasizing the molecular and cellular mechanisms of blood disorders and their treatments. The research on proteins involved in coagulation and immunity reflects a detailed examination of both basic science and potential therapeutic applications.

Best Publications

  • Extracellular histones are major mediators of death in sepsis

    Jun Xu;Xiaomei Zhang;Rosana Pelayo;Marc Monestier

  • Isolation of a membrane-bound cofactor for thrombin-catalyzed activation of protein C.

    N L Esmon;W G Owen;C T Esmon

  • Extracellular histones promote thrombin generation through platelet-dependent mechanisms: involvement of platelet TLR2 and TLR4

    Fabrizio Semeraro;Concetta T. Ammollo;James H. Morrissey;George L. Dale

  • Extracellular Histones Are Mediators of Death through TLR2 and TLR4 in Mouse Fatal Liver Injury

    Jun Xu;Xiaomei Zhang;Marc Monestier;Naomi L. Esmon

  • Thrombomodulin mutations in atypical hemolytic-uremic syndrome.

    Mieke Delvaeye;Marina Noris;Astrid De Vriese;Charles T. Esmon

  • Endotoxin enhances tissue factor and suppresses thrombomodulin expression of human vascular endothelium in vitro.

    K L Moore;S P Andreoli;N L Esmon;C T Esmon

  • Complex formation between thrombin and thrombomodulin inhibits both thrombin-catalyzed fibrin formation and factor V activation.

    C T Esmon;N L Esmon;K W Harris

  • Extracellular histones increase plasma thrombin generation by impairing thrombomodulin‐dependent protein C activation

    C. T. Ammollo;F. Semeraro;J. Xu;N. L. Esmon;N. L. Esmon

  • Thrombomodulin blocks the ability of thrombin to activate platelets.

    N L Esmon;R C Carroll;C T Esmon

  • Proteolytic formation and properties of gamma-carboxyglutamic acid-domainless protein C.

    N L Esmon;L E DeBault;C T Esmon

  • The interaction of a Ca2+-dependent monoclonal antibody with the protein C activation peptide region. Evidence for obligatory Ca2+ binding to both antigen and antibody.

    D J Stearns;S Kurosawa;P J Sims;N L Esmon

  • PAR1 cleavage and signaling in response to activated protein C and thrombin

    Matthew J. Ludeman;Hiroshi Kataoka;Yoga Srinivasan;Naomi L. Esmon

  • The crystal structure of the endothelial protein C receptor and a bound phospholipid.

    Vaheh Oganesyan;Natalia Oganesyan;Simon Terzyan;Dongfeng Qu

  • Metalloproteolytic Release of Endothelial Cell Protein C Receptor

    Jun Xu;Dongfeng Qu;Naomi L. Esmon;Naomi L. Esmon;Charles T. Esmon

  • The active site of thrombin is altered upon binding to thrombomodulin. Two distinct structural changes are detected by fluorescence, but only one correlates with protein C activation.

    Jia Ye;N. L. Esmon;C. T. Esmon;A. E. Johnson

  • Infection of vascular endothelial cells with herpes simplex virus enhances tissue factor activity and reduces thrombomodulin expression.

    Nigel S. Key;Gregory M. Vercellotti;John C. Winkelmann;Charles F. Moldow

  • Disruption of the endothelial cell protein C receptor gene in mice causes placental thrombosis and early embryonic lethality.

    Jian-Ming Gu;James T.B. Crawley;Gary Ferrell;Fangjiu Zhang

  • Overexpressing endothelial cell protein C receptor alters the hemostatic balance and protects mice from endotoxin

    W. Li;X. Zheng;J. Gu;J. Hunter

  • Endothelial protein C receptor.

    Charles T. Esmon;Jun Xu;Jian Ming Gu;Dongfeng Qu

  • Structural changes required for activation of protein C are induced by Ca2+ binding to a high affinity site that does not contain gamma-carboxyglutamic acid.

    Arthur E. Johnson;Naomi L. Esmon;Thomas M. Laue;Charles T. Esmon

Frequent Co-Authors

Charles T. Esmon
Charles T. Esmon Oklahoma Medical Research Foundation
Alireza R. Rezaie
Alireza R. Rezaie Oklahoma Medical Research Foundation
Wolfram Ruf
Wolfram Ruf Johannes Gutenberg University of Mainz
James H. Morrissey
James H. Morrissey University of Michigan–Ann Arbor
Denisa D. Wagner
Denisa D. Wagner Boston Children's Hospital
Thomas M. Laue
Thomas M. Laue University of New Hampshire
Florea Lupu
Florea Lupu Oklahoma Medical Research Foundation
Shaun R. Coughlin
Shaun R. Coughlin University of California, San Francisco
Philip W. Majerus
Philip W. Majerus Washington University in St. Louis
Arthur E. Johnson
Arthur E. Johnson Texas A&M University

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