Author

H. Willenbring

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

Biology Disciplines

Click to filter author papers

Bioengineering· 1 Pathology· 1 Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:human· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Organism:mouse· 1 Assay:organoid / primary culture· 1

Frequent Co-Authors

A. Laemmle· 1 shared A. N. Mattis· 1 shared B. Siemons· 1 shared C. C. Duwaerts· 1 shared C. L. Her· 1 shared C. S. Lee· 1 shared E. Miller· 1 shared F. T. Lee-Montiel· 1 shared

Activity by Year

2018-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperBioengineering

A. Laemmle

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Integrated hiPSC-based liver and heart microphysiological systems predict unsafe drug-drug interaction

F. T. Lee-Montiel, A. Laemmle, L. Dumont, C. S. Lee, N. Huebsch, V. Charwat, H. Okochi, M. J. Hancock, B. Siemons, S. C. Boggess, I. Goswami, E. Miller, H. Willenbring, K. Healy

The paper integrates hiPSC-based liver and heart microphysiological systems to predict drug-drug interactions, showing ketoconazole inhibits cisapride metabolism, causing arrhythmia in cardiac MPSs.

bioRxiv · May 24, 2020 · PreprintBioengineering

iPSC-derived hepatocytes from patients with nonalcoholic fatty liver disease display a disease-specific gene expression profile

C. C. Duwaerts, C. L. Her, N. J. Phillips, H. Willenbring, A. N. Mattis, J. J. Maher

The paper generates iPSC-derived hepatocytes from NAFLD patients to identify disease-specific gene expression profiles without metabolic challenge.

bioRxiv · Apr 20, 2020Pathology

Hepatocyte Nuclear Factor 4 alpha (HNF4α) Activation is Essential for Termination of Liver Regeneration

I. Huck, S. Gunewardena, R. Espanol-Suner, H. Willenbring, U. Apte

This study shows that HNF4α reexpression after liver injury is critical for hepatocytes to exit the cell cycle and resume function during liver regeneration.

bioRxiv · Apr 20, 2018Physiology