Author

H. Schenk

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 1 Ecology· 1 Evolutionary Biology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Approach:statistical model· 2 Organism:E. coli· 1 Organism:mouse· 1

Frequent Co-Authors

A. Traulsen· 1 shared E. Rousseau· 1 shared F. Njau· 1 shared G. Demarre· 1 shared G. Tran Van Nhieu· 1 shared H. Haller· 1 shared H. Schulenburg· 1 shared J. Menne· 1 shared

Activity by Year

2019-2019 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 10 mutual co-author links

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1 shared paperEvolutionary Biology

A. Traulsen

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4 papers

Recent·Most cited

How long do Red Queen dynamics survive under genetic drift? A comparative analysis of evolutionary and eco-evolutionary models

H. Schenk, H. Schulenburg, A. Traulsen

This study compares evolutionary and eco-evolutionary models of Red Queen dynamics, finding that ecological dynamics and local competition accelerate genotype extinction compared to fixed population size models.

bioRxiv · Dec 11, 2019Evolutionary Biology

Calcium dobesilate reduces VEGF signaling by interfering with heparan sulfate binding site and protects from vascular complications in diabetic mice

F. Njau, N. Shushakova, H. Schenk, V. C. Wulfmeyer, R. Bollin, J. Menne, H. Haller

This study shows calcium dobesilate inhibits VEGF signaling by blocking heparan sulfate binding, reducing vascular complications in diabetic mice.

bioRxiv · Jun 5, 2019Cell Biology

Bacteriophage can promote the emergence of physiologically sub-optimal host phenotypes

H. Schenk, M. Sieber

The paper models how bacteriophage dependence on host growth rate creates a feedback loop that allows slow-growing bacteria to outcompete fast-growing ones, potentially leading to phage extinction and altruistic host death.

bioRxiv · Apr 29, 2019 · PreprintEcology

The Crohn s disease-associated Escherichia coli strain LF82 rely on SOS and stringent responses to survive, multiply and tolerate antibiotics within macrophages.

G. Demarre, V. Prudent, H. Schenk, E. Rousseau, M.-A. Bringer, N. Barnich, G. Tran Van Nhieu, S. Rimsky, S. De Monte, O. Espeli

This study investigates how AIEC LF82 survives and multiplies in macrophages, revealing phenotypic switches and antibiotic tolerance mechanisms.

bioRxiv · Feb 27, 2019Microbiology