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Mechanism of Action at the Molecular Level of the Antiviral Drug 3(2H)-Isoflavene against Type 2 Poliovirus. Anna L. Salvati, 2004.The mechanism of action of the antiviral compound 3(2H)-isoflavene against Sabin type 2 poliovirus has been studied, and interference with virus uncoating was demonstrated . Isolation and sequencing of drug-resistant variants revealed single amino acid substitutions (I194M or D131V) in the VP1 capsid protein . While M194 is located in a hydrophobic pocket and should partially fill the space occupied by the isoflavene ring, V131 is exposed on the VP1 surface, forming a contact with VP4 . The D131V mutation most likely induces local conformational changes in VP1 and/or VP4 that affect viral flexibility . Two dependent variants, N53S of VP1 and K58E of VP4, both located on the inner surface of the capsid, near the threefold axis of symmetry, were also selected . Both mutations affected viral stability, allowing the transition to 135S particles in the absence of drug, without the involvement of the viral receptor . Cold Shock Induction of the cspL Gene in Lactobacillus plantarum Involves Transcriptional Regulation. Sylviane Derzelle, 2002.Fragments of the cspL promoter region were fused to the gusA reporter and reintroduced into Lactobacillus plantarum cells, either on multicopy plasmids or through single-copy chromosomal integration . ß-Glucuronidase activity and primer extension data demonstrate that the cspL promoter is induced in response to cold shock and that multicopy constructs quench the induction of the resident cspL gene . Osmoregulation in the Parasitic Protozoan Tritrichomonas foetus. Sarah L. Maroulis, 2003.Tritrichomonas foetus was shown to undergo a regulatory volume increase (RVI) when it was subjected to hyperosmotic challenge, but there was no regulatory volume decrease after hypoosmotic challenge, as determined by using both light-scattering methods and measurement of intracellular water space to monitor cell volume . An investigation of T . foetus intracellular amino acids revealed a pool size (65 mM) that was similar to that of Trichomonas vaginalis but was considerably smaller than those of Giardia intestinalis and Crithidia luciliae . Changes in amino acid concentrations in response to hyperosmotic challenge were found to account for only 18% of the T . foetus RVI . The T . foetus intracellular sodium and potassium concentrations were determined to be 35 and 119 mM, respectively . The intracellular K+ concentration was found to increase considerably during exposure to hyperosmotic stress, and, assuming that there was a monovalent accompanying anion, this increase was estimated to account for 87% of the RVI . By using light scattering it was determined that the T . foetus RVI was enhanced by elevated external K+ concentrations and was inhibited when K+ and/or Cl- was absent from the medium . The results suggested that the well-documented Na+-K+-2Cl- cotransport system was responsible for the K+ influx activated during the RVI . However, inhibitors of Na+-K+-2Cl- cotransport in other systems, such as quinine, ouabain, furosemide, and bumetanide, had no effect on the RVI or K+ influx in T . foetus .
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