tularemia/tyrosine

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The significance and mechanism of an increased serum phenylalanine-tyrosine ratio during infection.

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Infections or inflammatory states often cause significant increases in serum phenylalanine and the phenylalanine-tyrosine ratio. More than 95% of samples obtained during inflammatory diseases in man showed phenylalanine-tyrosine ratio increases greater than the maximum normal values. An increase in

Changes in whole blood and serum components of grivet monkeys with experimental respiratory Francisella tularensis infection.

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Grivet monkeys infected with virulent Francisella tularensis Strain Schu S4 showed significant early changes in serum levels of trace metals, triglycerides and activities of alkaline phosphatase, lactate dehydrogenase and alpha-hydroxybutyrate dehydrogenase. Free amino acid levels decreased slightly

The tyrosine kinase Syk promotes phagocytosis of Francisella through the activation of Erk.

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Francisella tularensis is a highly infectious, Gram-negative intra-cellular pathogen that can cause the zoonotic disease tularemia. Although the receptors critical for internalization of Francisella by macrophages are beginning to be defined, the identity of the downstream signaling pathways

Cell biology and molecular ecology of Francisella tularensis.

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Francisella tularensis is a highly infectious intracellular bacterium that causes the fulminating disease tularemia, which can be transmitted between mammals by arthropod vectors. Genomic studies have shown that the F. tularensis has been undergoing genomic decay with the most virulent strains

The role of MAPK signal pathways during Francisella tularensis LVS infection-induced apoptosis in murine macrophages.

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Francisella tularensis is a highly virulent intracellular pathogen responsible for tularemia. This bacterium is capable of infecting many mammalian species and various cell types, but little is known about the mechanisms of survival and interactions with host cells. We examined the number of

Structure and function of REP34 implicates carboxypeptidase activity in Francisella tularensis host cell invasion.

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Francisella tularensis is the etiological agent of tularemia, or rabbit fever. Although F. tularensis is a recognized biothreat agent with broad and expanding geographical range, its mechanism of infection and environmental persistence remain poorly understood. Previously, we identified seven F.

Francisella tularensis invasion of lung epithelial cells.

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Francisella tularensis, a gram-negative facultative intracellular bacterial pathogen, causes disseminating infections in humans and other mammalian hosts. Macrophages and other monocytes have long been considered the primary site of F. tularensis replication in infected animals. However, recently it

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