Author

Daniel T. Infield

University of IowaORCID 0009-0004-5295-484XUnclaimed ORCID profile · follow to get notified of new preprints

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Daniel T. Infield1 paper

Biology Disciplines

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Molecular Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1 Assay:electrophysiology· 1 Organism:human· 1 Assay:proteomics· 1

Frequent Co-Authors

Christopher A. AherniD· 2 shared Adam L. Mackey· 1 shared Alex DouiD· 1 shared Alfredo Perales‐PuchaltiD· 1 shared Barry LondoniD· 1 shared Bum‐Rak ChoiiD· 1 shared Christian Anderson· 1 shared Colin J. ClarkiD· 1 shared

Activity by Year

2019-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersPhysiology

Christopher A. AhernORCID

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2 papers

Recent·Most cited

Non-canonical Sodium Channel Isoforms Underlie Chamber Specific Cardiac Excitability

Colin J. Clark, Christian Anderson, Alex Dou, Jason M. Dierdorff, Jason D. Galpin, Lionel Gissot, Samantha L. Thompson, Hannah Choi, Jin‐Young Yoon, Daniel T. Infield, Jared M. McLendon, Peter Bronk, Keane Leeds, Ryan L. Boudreau, Bum‐Rak Choi, , Christopher A. Ahern

This study identifies chamber-specific contributions of non-NaV1.5 sodium channel isoforms to cardiac excitability using a chemical-genetic mouse model and electrophysiological recordings.

bioRxiv · Aug 27, 2025 · PreprintPhysiology

Engineered transfer RNAs for suppression of premature termination codons

John D. Lueck, Jae Seok Yoon, Alfredo Perales‐Puchalt, Adam L. Mackey, Daniel T. Infield, Mark A. Behlke, Marshall R. Pope, David B. Weiner, William R. Skach, Paul B. McCray, Christopher A. Ahern

This paper identifies engineered transfer RNAs (ACE-tRNA) that suppress premature termination codons in mammalian cells and mice, showing high suppression activity for common disease-causing nonsense codons.

Nature Communications · Feb 18, 2019Peer-reviewedMolecular Biology