Author

Felicia Deng

University of Wisconsin–Madison

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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Biochemistry· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Approach:experimental assay· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1 Assay:metabolomics· 1

Frequent Co-Authors

Jing FaniD· 2 shared Nicholas L. ArpiD· 2 shared Steven V JohniD· 2 shared Anna Huttenlocher AiD· 1 shared Bridget E. ShieldsiD· 1 shared Carlos Mellado FritziD· 1 shared Daniel Amador‐NogueziD· 1 shared Gretchen L. SeimiD· 1 shared

Activity by Year

2026-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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Curved chords = mutual co-authorship

2 shared papersImmunology

Jing FanORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Multi-omic analysis reveals nitric oxide dependent remodeling in classically activated macrophages and identifies negative regulation mediated by AKR1A1

Nicholas L. Arp, Uzziah S. Urquiza, Marcel Morgenstern, Jonathan H. Schrope, James A. Votava, Steven V John, Jack J Stevens, Felicia Deng, Anna Huttenlocher A, Joshua J. Coon, Jing Fan

This study uses multi-omic analysis to show NO* drives controlled remodeling in macrophages, with AKR1A1 mediating negative regulation of metabolic and functional changes during immune response.

Redox Biology · Apr 22, 2026Peer-reviewedImmunology

Discovery of metabolites produced by reactions between central carbon metabolites and cysteine that mark inflammatory macrophages

Nicholas L. Arp, Felicia Deng, Jorgo Lika, Gretchen L. Seim, Paulo Falco Cobra, Carlos Mellado Fritz, Steven V John, Swetha Rathinaraj, Bridget E. Shields, Daniel Amador‐Noguez, Katherine A. Henzler‐Wildman, Jing Fan

The paper identifies sulfur-containing metabolites specific to inflammatory macrophages, showing they are produced from cysteine and central metabolism intermediates and are elevated in human inflammatory lesions.

bioRxiv · Mar 20, 2026 · PreprintBiochemistry