Author

Cole R. Michel

University of Colorado AnschutzORCID 0000-0002-9058-7495Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Developmental Biology· 1 Genetic & Genomic Medicine· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Research Focus:cell type annotation· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Organism:mouse· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

Christopher J. Hill· 1 shared Claudia Soler‐AlfonsoiD· 1 shared Daniella Helena HockiD· 1 shared David A. StroudiD· 1 shared Dustin BaldridgeiD· 1 shared Dylan SarbaughiD· 1 shared Eric TyckseniD· 1 shared Erin E. ConboyiD· 1 shared

Activity by Year

2025-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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1 shared paperDevelopmental Biology

Christopher J. Hill

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Dominant negative ATP5F1A variants disrupt oxidative phosphorylation causing neurological disorders

Sara M. Fielder, Marisa W. Friederich, Daniella Helena Hock, Jessie R. Zhang, Liana Valin, Jill Anne Rosenfeld, Kevin T. A. Booth, Natasha J. Brown, Rocío Rius, Tanavi Sharma, Liana N. Semcesen, Kim C. Worley, Lindsay Catherine Burrage, Kayla M. Treat, Tara E. Samson, , Stephen C. Pak

This study identifies de novo ATP5F1A variants causing neurological disorders through dominant negative mechanisms, expanding the known phenotypic and genotypic spectrum of complex V deficiency.

EMBO Molecular Medicine · Aug 26, 2025Peer-reviewedGenetic & Genomic Medicine

CHD4 and NKX2.2 Cooperate to Regulate Beta Cell Function by Repressing Non-Beta Cell Gene Programs

Dylan Sarbaugh, Thais Gaia Oliveira, Michelle A. Guney, McKenna R. Casey, Victoria M. Hoelscher, Christopher J. Hill, Cole R. Michel, Kristen L. Wells, Richard K.P. Benninger, Lori Sussel

This study identifies CHD4 as a cofactor of NKX2.2 that regulates beta cell function by repressing non-beta cell gene programs, leading to diabetes when disrupted.

bioRxiv · Jun 16, 2025 · PreprintDevelopmental Biology