Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of cultured bovine carotid artery endothelial cells with 10(-7) M plasmin increased the cellular diacylglycerol which was determined by the formation of [3H]palmitate-labeled diacylglycerol and diacylglycerol mass. Upon the stimulation with plasmin, a gradual increase in diacylglycerol formation was observed within 20 min then slightly declined. The maximal effect during the 1-h time course study was 45 and 55% increases in [3H]palmitate-labeled diacylglycerol and diacylglycerol mass, respectively, at 20 min after plasmin treatment. Formation of phosphatidylethanol was also studied in [3H]palmitate-prelabeled cells in the presence of ethanol. Treatment with plasmin for 20 min induced a significant 45% increase in phosphatidylethanol formation. The present results indicate that the plasmin-induced diacylglycerol formation in endothelial cells was at least in part mediated through the phospholipase D activation.
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PMID:Diacylglycerol formation induced by human plasmin in cultured endothelial cells. 781 64

The authors were the first to perform stimulation of parasitizing condition of plague bacilli in mammalian bloodstream by addition of adequate quantity of glucose and calcium ions into the routine bacteriological medium, as well as growing the plague agent in RPMI-1640, isotonic to the serum of man and mammals susceptible to plague. Comparison of proliferative, phenotypic, and biochemical properties of fully virulent and vaccine Y. pestis strains demonstrated the advantages of RPMI-1640 medium, which provided extensive in vitro multiplication of the mentioned microorganisms similar to the bacterioemic stage of plague. Using methods of molecular microbiology and immunology, including a panel of monoclonal antibodies, the researchers demonstrated an abrupt fall of production of main plague surface species-specific antigens such as F1, 'murine' toxin/phospholipase D and fibrinolysin, followed by inhibition of biochemical activities associated with these antigenic substances in Y. pestis, as well as specific components of lipopolysaccharide. Possible molecular mechanisms of virulence and adaptive variability of plague bacteria in the extracellular conditions in mammalian organism are discussed.
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PMID:[Extracellular resistance of Yersinia pestis to phagocytosis]. 1632 Jul 2