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Andreas Haldimann

Researcher at Purdue University

Publications -  11
Citations -  1521

Andreas Haldimann is an academic researcher from Purdue University. The author has contributed to research in topics: Plasmid & Response regulator. The author has an hindex of 9, co-authored 11 publications receiving 1466 citations. Previous affiliations of Andreas Haldimann include Oregon Health & Science University.

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Conditional-Replication, Integration, Excision, and Retrieval Plasmid-Host Systems for Gene Structure-Function Studies of Bacteria

TL;DR: A series of powerful and versatile conditional-replication, integration, and modular (CRIM) plasmids that encode different forms of resistance and can be used together in the same cell for stable expression of complex metabolic or regulatory pathways from diverse sources are developed.
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Conditionally replicative and conjugative plasmids carrying lacZ alpha for cloning, mutagenesis, and allele replacement in bacteria.

TL;DR: Several new cloning vectors for mutagenesis and allele replacement experiments are described, including plasmids that have the R6K gamma DNA replication origin so they replicate only in bacteria supplying the pi replication protein, and which also encode a positive counterselectable marker.
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Use of new methods for construction of tightly regulated arabinose and rhamnose promoter fusions in studies of the Escherichia coli phosphate regulon.

TL;DR: By using P(araB)-phoB+, P(rhaB)- phoB+ or P-rhaB-phoR+ fusions, this work was able to overcome the extremely deleterious growth defect of a Pst+ delta phoU mutant and indicates that less PhoR than PhoB is required for transcriptional activation of the Pho regulon, which is consistent with their respective modes of action.
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Transcriptional regulation of the Enterococcus faecium BM4147 vancomycin resistance gene cluster by the VanS-VanR two-component regulatory system in Escherichia coli K-12.

TL;DR: An Escherichia coli K-12 model system was developed for studying the VanS-VanR two-component regulatory system required for high-level inducible vancomycin resistance in Enterococcus faecium BM4147 and it was demonstrated that the response regulator VanR activates PvanH, but not PvanR, expression upon activation (phosphorylation) by the partner kinase VanS.
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Altered recognition mutants of the response regulator PhoB: A new genetic strategy for studying protein–protein interactions

TL;DR: The overall genetic strategy described here may be useful for studying interactions of other components of the vancomycin resistance and P1 signal transduction pathways, other two-component regulatory systems, and other interacting proteins.