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Curt R. Fischer

Researcher at Stanford University

Publications -  59
Citations -  3508

Curt R. Fischer is an academic researcher from Stanford University. The author has contributed to research in topics: Escherichia coli & Mutant. The author has an hindex of 22, co-authored 56 publications receiving 2809 citations. Previous affiliations of Curt R. Fischer include University of California & Tokyo Institute of Technology.

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Tuning genetic control through promoter engineering

TL;DR: The characterized library of promoters is used to assess the impact of phosphoenolpyruvate carboxylase levels on growth yield and deoxy-xylulose-P synthase Levels on lycopene production and is illustrated as being generalizable to eukaryotic organisms and thus constitutes an integral platform for functional genomics, synthetic biology, and metabolic engineering endeavors.
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Selection and optimization of microbial hosts for biofuels production.

TL;DR: This paper examines the prospects for bioproduction of four second-generation biofuels (n-butanol, 2- butanol, terpenoids, or higher lipids) from four feedstocks (sugars and starches, lignocellulosics, syngas, and atmospheric carbon dioxide) and tests seven fast-growing host organisms for tolerance to production stresses.
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Engineering of Promoter Replacement Cassettes for Fine-Tuning of Gene Expression in Saccharomyces cerevisiae

TL;DR: The detailed characterization of the yeast promoter collection comprising 11 mutants of the strong constitutive Saccharomyces cerevisiae TEF1 promoter is provided, allowing detailed genotype-phenotype characterizations.
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Coevolution of Bacteriophage PP01 and Escherichia coli O157:H7 in Continuous Culture

TL;DR: Cessation of major outer membrane protein OmpC production and alteration of lipopolysaccharide composition enabled E. coli O157:H7 to escape PP01 infection.
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N-hydroxy-pipecolic acid is a mobile metabolite that induces systemic disease resistance in Arabidopsis

TL;DR: It is shown that N-hydroxy-pipecolic acid metabolites are mobile defense signals produced at the site of bacterial infection and establish and amplify defense in uninfected, distal tissues and suggests that the N-OH-Pip pathway is a promising target for metabolic engineering to enhance disease resistance.