Antoine H. Dufour, Ph.D.
Affiliations: | 2010 | Chemistry | Stony Brook University, Stony Brook, NY, United States |
Area:
Pharmaceutical Chemistry, Biochemistry, OncologyGoogle:
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Parents
Sign in to add mentorNicole S. Sampon | grad student | 2010 | SUNY Stony Brook | |
(The role of the hemopexin domain of matrix metalloproteinases in cell migration.) |
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Publications
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de Almeida LGN, Thode H, Eslambolchi Y, et al. (2022) Matrix Metalloproteinases: From Molecular Mechanisms to Physiology, Pathophysiology, and Pharmacology. Pharmacological Reviews. 74: 712-768 |
Wang L, Main K, Wang H, et al. (2021) Biochemical Tools for Tracking Proteolysis. Journal of Proteome Research |
Menon NG, Goyal R, Lema C, et al. (2021) Proteoglycan 4 (PRG4) expression and function in dry eye associated inflammation. Experimental Eye Research. 108628 |
Das N, Benko C, Gill SE, et al. (2020) The Pharmacological TAILS of Matrix Metalloproteinases and Their Inhibitors. Pharmaceuticals (Basel, Switzerland). 14 |
Fallata AM, Wyatt RA, Levesque JM, et al. (2019) Intracellular Localization in Zebrafish Muscle and Conserved Sequence Features Suggest Roles for Gelatinase A Moonlighting in Sarcomere Maintenance. Biomedicines. 7 |
Young D, Das N, Anowai A, et al. (2019) Matrix Metalloproteases as Influencers of the Cells' Social Media. International Journal of Molecular Sciences. 20 |
Chopra S, Overall CM, Dufour A. (2019) Matrix metalloproteinases in the CNS: interferons get nervous. Cellular and Molecular Life Sciences : Cmls |
Mallia-Milanes B, Dufour A, Philp C, et al. (2018) TAILS proteomics reveals dynamic changes in airway proteolysis controlling protease activity and innate immunity during COPD exacerbations. American Journal of Physiology. Lung Cellular and Molecular Physiology |
Dufour A, Bellac CL, Eckhard U, et al. (2018) C-terminal truncation of IFN-γ inhibits proinflammatory macrophage responses and is deficient in autoimmune disease. Nature Communications. 9: 2416 |
Jagdeo JM, Dufour A, Klein T, et al. (2018) N-Terminomics TAILS identifies host cell substrates of poliovirus and coxsackievirus B3 3C proteinases that modulate virus infection. Journal of Virology |