C
Clare Cooksley
Researcher at University of Adelaide
Publications - 56
Citations - 1739
Clare Cooksley is an academic researcher from University of Adelaide. The author has contributed to research in topics: Staphylococcus aureus & Biofilm. The author has an hindex of 16, co-authored 45 publications receiving 1507 citations. Previous affiliations of Clare Cooksley include Queen's University & University of Nottingham.
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Journal ArticleDOI
The ClosTron: Mutagenesis in Clostridium refined and streamlined.
John T. Heap,Sarah A. Kuehne,Muhammad Ehsaan,Stephen T. Cartman,Clare Cooksley,Jamie C. Scott,Nigel P. Minton +6 more
TL;DR: The improved ClosTron system supersedes the prototype plasmid pMTL007 and the original method, and exploits the potential of Group II introns more fully, and means mutants can now be constructed with very little time and effort for the researcher.
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Integration of DNA into bacterial chromosomes from plasmids without a counter-selection marker
John T. Heap,Muhammad Ehsaan,Clare Cooksley,Yen-Kuan Ng,Stephen T. Cartman,Klaus Winzer,Nigel P. Minton +6 more
TL;DR: Novel DNA integration strategies are explored that exploit activation or inactivation of genes leading to a selectable phenotype, and asymmetrical regions of homology to control the order of recombination events to open the way to reliable integration of DNA including large synthetic constructs in diverse microorganisms.
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Association between Group 2 Innate Lymphoid Cells enrichment, nasal polyps and allergy in Chronic Rhinosinusitis
Dijana Miljkovic,Ahmed Bassiouni,Clare Cooksley,Judy Ou,Ehud Hauben,Peter J. Wormald,Sarah Vreugde +6 more
TL;DR: The ILC2 compartment in CRS is characterized by investigating the correlations between I LC2s, Th2 cells and Th2 cytokines expression in C RS patients by investigatingThe correlations betweenILC2S, Th1 cells andTh2 cytokine expression in patients with chronic rhinosinusitis.
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Targeted mutagenesis of the Clostridium acetobutylicum acetone-butanol-ethanol fermentation pathway.
TL;DR: Unexpectedly, bdhA and bdhB mutants did not affect solvent production, whereas inactivation of the previously uncharacterised putative alcohol dehydrogenase CAP0059 resulted in increased acetone, butanol, and ethanol formation, which reinforces the need for mutant complementation and Southern Blot analysis.
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NapA protects Helicobacter pylori from oxidative stress damage, and its production is influenced by the ferric uptake regulator.
TL;DR: It is demonstrated that repression of NapA production by iron starvation was not so pronounced in a H. pylori fur mutant, suggesting that the ferric uptake regulator (Fur) is involved in napA regulation, and a potential fur box by which this control could be mediated is identified.