Author

B. Willingham

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

Physiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Research Focus:metabolism & bioenergetics· 1 Organism:mouse· 1

Frequent Co-Authors

A. C. Abraham· 1 shared B. Glancy· 1 shared C. Liu· 1 shared C. S. Davis· 1 shared D. Harden· 1 shared E. Ganji· 1 shared I. Bhattacharya· 1 shared L. Iannucci· 1 shared

Activity by Year

2024-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 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 paperPhysiology

A. C. Abraham

Mutual co-authors in cluster

Author profile →

1 paper

Recent·Most cited

Overexpression of enhanced yellow fluorescent protein fused with Channelrhodopsin-2 causes contractile dysfunction in skeletal muscle

S. N. E. Lamia, C. S. Davis, P. C. D. Macpherson, B. Willingham, Y. Zhang, C. Liu, L. Iannucci, E. Ganji, D. Harden, I. Bhattacharya, A. C. Abraham, S. V. Brooks, B. Glancy, M. L. Killian

This study shows that overexpressing ChR2-EYFP in skeletal muscle causes contractile dysfunction, while ChR2-only mice show normal function, highlighting the need for alternative optogenetic models.

bioRxiv · Jun 6, 2024Physiology