K
Knut Jahreis
Researcher at University of Osnabrück
Publications - 34
Citations - 1776
Knut Jahreis is an academic researcher from University of Osnabrück. The author has contributed to research in topics: Catabolite repression & PEP group translocation. The author has an hindex of 23, co-authored 34 publications receiving 1704 citations. Previous affiliations of Knut Jahreis include University of Utah.
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Journal ArticleDOI
A quantitative approach to catabolite repression in Escherichia coli.
Katja Bettenbrock,Sophia Fischer,Andreas Kremling,Knut Jahreis,Thomas Sauter,Ernst Dieter Gilles +5 more
TL;DR: The different phenomena affecting the phosphorylation level of EIIACrr, the key regulation molecule for inducer exclusion and catabolite repression in enteric bacteria, can now be explained quantitatively.
Journal ArticleDOI
Correlation between Growth Rates, EIIACrr Phosphorylation, and Intracellular Cyclic AMP Levels in Escherichia coli K-12
Katja Bettenbrock,Thomas Sauter,Thomas Sauter,Knut Jahreis,Andreas Kremling,Joseph W. Lengeler,Ernst Dieter Gilles +6 more
TL;DR: The relation between cellular growth rates and the key parameters of catabolite repression were increasingly uncoupled from the growth rate, which perhaps indicates an increasing role executed by other global control systems, in particular the stringent-relaxed response system.
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Coupling the phosphotransferase system and the methyl-accepting chemotaxis protein-dependent chemotaxis signaling pathways of Escherichia coli.
TL;DR: It is found that in mutant strains HPr-like proteins could substitute for HPr in transport but did not mediate chemotactic signaling, suggesting the following model for signal transduction in PTS-dependent chemotaxis.
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Ins and outs of glucose transport systems in eubacteria.
TL;DR: This review aims to provide an overview of glucose uptake systems found in the eubacterial kingdom and highlight the diverse and sophisticated regulatory features of glucose transport systems.
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Glucose transporter mutants of Escherichia coli K-12 with changes in substrate recognition of IICB(Glc) and induction behavior of the ptsG gene.
TL;DR: A new regulatory mechanism involved in ptsG induction is postulated, which modulates IIC(Glc) which controls the repressor DgsA and hence ptsG expression and, by the same mechanism, glucose uptake and phosphorylation also control the expression of the pts operon and probably of all operons controlled by the represses.