Abstract
The induction of a unique macrophage procoagulant molecule by murine hepatitis virus strain 3 correlates with the severity of viral hepatitis. The role of tyrosine phosphorylation in the signalling pathway leading to procoagulant expression was studied. Murine hepatitis virus strain 3 initiated a rapid increase in phosphotyrosine accumulation. Tyrosine kinase inhibition precluded this increase and abrogated expression of the virus-induced procoagulant mouse fibrinogen-like protein (musfiblp) gene. These findings suggest that manipulation of this signalling pathway in vivo might represent a novel approach to treating this disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzoquinones
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Catechols / pharmacology
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Cells, Cultured
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Female
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Genistein
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Hepatitis, Viral, Animal / immunology
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Hepatitis, Viral, Animal / physiopathology
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Isoflavones / pharmacology
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Kinetics
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Lactams, Macrocyclic
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Macrophages, Peritoneal / drug effects
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Macrophages, Peritoneal / physiology*
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Macrophages, Peritoneal / virology
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Mice
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Murine hepatitis virus / classification
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Murine hepatitis virus / physiology*
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Nitriles / pharmacology
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Phosphorylation
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Phosphotyrosine
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Protein-Tyrosine Kinases / antagonists & inhibitors
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Protein-Tyrosine Kinases / metabolism*
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Quinones / pharmacology
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Rifabutin / analogs & derivatives
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Tyrosine / analogs & derivatives
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Tyrosine / metabolism*
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Tyrphostins*
Substances
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Benzoquinones
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Catechols
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Isoflavones
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Lactams, Macrocyclic
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Nitriles
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Quinones
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Tyrphostins
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tyrphostin 47
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Rifabutin
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Phosphotyrosine
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Tyrosine
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herbimycin
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Genistein
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Protein-Tyrosine Kinases