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Dickson D 《Science (New York, N.Y.)》1982,217(4555):134-135
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Discovery and directed evolution of a glyphosate tolerance gene 总被引:2,自引:0,他引:2
Castle LA Siehl DL Gorton R Patten PA Chen YH Bertain S Cho HJ Duck N Wong J Liu D Lassner MW 《Science (New York, N.Y.)》2004,304(5674):1151-1154
The herbicide glyphosate is effectively detoxified by N-acetylation. We screened a collection of microbial isolates and discovered enzymes exhibiting glyphosate N-acetyltransferase (GAT) activity. Kinetic properties of the discovered enzymes were insufficient to confer glyphosate tolerance to transgenic organisms. Eleven iterations of DNA shuffling improved enzyme efficiency by nearly four orders of magnitude from 0.87 mM-1 min-1 to 8320 mM-1 min-1. From the fifth iteration and beyond, GAT enzymes conferred increasing glyphosate tolerance to Escherichia coli, Arabidopsis, tobacco, and maize. Glyphosate acetylation provides an alternative strategy for supporting glyphosate use on crops. 相似文献
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Johansson L Rytkonen A Bergman P Albiger B Källström H Hökfelt T Agerberth B Cattaneo R Jonsson AB 《Science (New York, N.Y.)》2003,301(5631):373-375
The human-specific bacterial pathogen Neisseria meningitidis is a major cause of sepsis and/or meningitis. The pili of N. meningitidis interact with CD46, a human cell-surface protein involved in regulation of complement activation. Transgenic mice expressing human CD46 were susceptible to meningococcal disease, because bacteria crossed the blood-brain barrier in these mice. Development of disease was more efficient with piliated bacteria after intranasal, but not intraperitoneal, challenge of CD46 transgenic mice, suggesting that human CD46 facilitates pilus-dependent interactions at the epithelial mucosa. Hence, the human CD46 transgenic mice model is a potentially useful tool for studying pathogenesis and for vaccine development against meningococcal disease. 相似文献
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Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP 总被引:2,自引:0,他引:2
Lewis J Dickson DW Lin WL Chisholm L Corral A Jones G Yen SH Sahara N Skipper L Yager D Eckman C Hardy J Hutton M McGowan E 《Science (New York, N.Y.)》2001,293(5534):1487-1491
JNPL3 transgenic mice expressing a mutant tau protein, which develop neurofibrillary tangles and progressive motor disturbance, were crossed with Tg2576 transgenic mice expressing mutant beta-amyloid precursor protein (APP), thus modulating the APP-Abeta (beta-amyloid peptide) environment. The resulting double mutant (tau/APP) progeny and the Tg2576 parental strain developed Abeta deposits at the same age; however, relative to JNPL3 mice, the double mutants exhibited neurofibrillary tangle pathology that was substantially enhanced in the limbic system and olfactory cortex. These results indicate that either APP or Abeta influences the formation of neurofibrillary tangles. The interaction between Abeta and tau pathologies in these mice supports the hypothesis that a similar interaction occurs in Alzheimer's disease. 相似文献
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