K
K. Mark Coggeshall
Researcher at Oklahoma Medical Research Foundation
Publications - 38
Citations - 2377
K. Mark Coggeshall is an academic researcher from Oklahoma Medical Research Foundation. The author has contributed to research in topics: Bacillus anthracis & Cytokine. The author has an hindex of 26, co-authored 38 publications receiving 2025 citations. Previous affiliations of K. Mark Coggeshall include University of Oklahoma.
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Journal ArticleDOI
Hexokinase Is an Innate Immune Receptor for the Detection of Bacterial Peptidoglycan
Andrea J. Wolf,Christopher N. Reyes,Wenbin Liang,Courtney A. Becker,Kenichi Shimada,Matthew L. Wheeler,Hee Cheol Cho,Narcis I. Popescu,K. Mark Coggeshall,Moshe Arditi,David M. Underhill +10 more
TL;DR: This study shows that a metabolic enzyme can act as a pattern recognition receptor and is caused by release of N-acetylglucosamine that is detected in the cytosol by the glycolytic enzyme hexokinase.
Journal ArticleDOI
TREM2- and DAP12-dependent activation of PI3K requires DAP10 and is inhibited by SHIP1.
Qisheng Peng,Qisheng Peng,Shikha Malhotra,James A. Torchia,William G. Kerr,K. Mark Coggeshall,Mary Beth Humphrey,Mary Beth Humphrey +7 more
TL;DR: A previously uncharacterized interaction of SHIP1 with DAP12 is demonstrated that functionally limits TREM2- and DAP 12-dependent signaling and a mechanism through which SHIP 1 regulates key ITAM-containing receptors by directly blocking the binding and activation of PI3K is identified.
Journal ArticleDOI
IL-6 increases B-cell IgG production in a feed-forward proinflammatory mechanism to skew hematopoiesis and elevate myeloid production.
Kenichiro Maeda,Harshini Mehta,Harshini Mehta,Douglas A. Drevets,K. Mark Coggeshall,K. Mark Coggeshall +5 more
TL;DR: The data indicate a feed-forward process in which peripheral macrophages, responding through IgG receptors to secreted IgG, produce IL-6, to support further B-cell production of IgG.
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Crosstalk between the coagulation and complement systems in sepsis.
TL;DR: Overall, this work demonstrates that live bacteria and bacterial products activate the complement and coagulation cascades, and that blocking formation of complement activation products, especially during the organ failure stage of severe sepsis could be a potentially important therapeutic strategy.
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Convergence of signaling pathways on the activation of ERK in B cells.
TL;DR: It is shown that the PI 3-kinase and Ras signaling cascades are intimately connected in B cells and that the activation of ERK is a signal integration point, since it requires simultaneous input from all three major signaling pathways.