Author

T. U. Esser

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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Bioengineering· 1 Biophysics· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Research Focus:drug response / drug discovery· 1 Organism:human· 1 Organism:mouse· 1 Assay:organoid / primary culture· 1

Frequent Co-Authors

B. Fabry· 2 shared D. Kah· 2 shared F. B. Engel· 2 shared A. Anspach· 1 shared A.-K. Guenther· 1 shared C. A. Dessalles· 1 shared C. Wiedwald· 1 shared D. Boehringer· 1 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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2 shared papersBiophysics

B. Fabry

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Contractility of cardiac and skeletal muscle tissue increases with environmental stiffness

D. Kah, J. Lell, T. Wach, M. Spoerrer, C. A. Dessalles, J. Kraxner, S. Wiedenmann, R. C. Gerum, S. Vergarajauregui, T. U. Esser, D. Boehringer, F. B. Engel, I. Thievessen, B. Fabry

This study shows that contractile force in cardiac and skeletal muscle tissues increases with environmental stiffness following a power-law relationship.

bioRxiv · Feb 23, 2024 · PreprintBiophysics

Direct 3D-bioprinting of hiPSC-derived cardiomyocytes to generate functional cardiac tissues

T. U. Esser, A. Anspach, K. A. Muenzebrock, D. Kah, S. Schruefer, J. Schenk, K. G. Heinze, D. W. Schubert, B. Fabry, F. B. Engel

This paper describes a method to directly 3D-bioprint hiPSC-derived cardiomyocytes into functional cardiac tissues that contract and respond to pharmacological stimulation.

bioRxiv · Jun 12, 2023Bioengineering

Transcription factor TAp73 and microRNA-449 complement each other to support multiciliogenesis

M. Wildung, T. U. Esser, K. B. Grausam, C. Wiedwald, L. Volceanov-Hahn, D. Riedel, S. Beuermann, L. Li, J. L. S. Zylla, A.-K. Guenther, M. Wienken, E. Ercetin, Z. Han, F. Bremmer, O. Shomroni, , M. Lize

The paper shows TAp73 and miR449 work together to support multiciliogenesis, with their combined loss causing brain defects and hydrocephalus.

bioRxiv · Dec 19, 2018Cell Biology