Author

Truman Kula

Wayne State University

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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Neuroscience· 3

Signature Assays, Organisms & Methods

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Organism:Drosophila· 3 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:differential expression· 1 Assay:proteomics· 1

Frequent Co-Authors

Kristin RichardsoniD· 3 shared Matthew V. PriftiiD· 3 shared Sokol V. TodiiD· 3 shared Fatimah H Hussein· 2 shared Anna StephaniD· 1 shared Anthony A. HighiD· 1 shared Autumn Jackson-Butler· 1 shared Fabio DemontisiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersNeuroscience

Kristin RichardsonORCID

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3 papers

Recent·Most cited

Androgen Receptor SUMO site mutations ameliorate toxicity in Drosophila models of SBMA

Kristin Richardson, Matthew V. Prifti, Truman Kula, Fatimah H Hussein, Sokol V. Todi

This study shows that mutating SUMOylation sites in the androgen receptor in Drosophila models of SBMA improves longevity but has limited effects on motor performance.

bioRxiv · Oct 24, 2026 · PreprintNeuroscience

Polyglutamine-expanded TBP rewires neuronal and muscle proteomes beyond transcription in a Drosophila model of SCA17

Matthew V. Prifti, Kristin Richardson, Fatimah H Hussein, Truman Kula, Anna Stephan, Yong-Dong Wang, Wei Wang, Anthony A. High, Suresh Poudel, Fabio Demontis, Sokol V. Todi

This study identifies tissue-specific proteomic changes in a Drosophila SCA17 model, showing polyglutamine-expanded TBP affects pathways beyond transcription.

bioRxiv · Oct 21, 2026 · PreprintNeuroscience

Insights into Dentatorubral-Pallidoluysian Atrophy from a new Drosophila model of disease

Matthew V. Prifti, Oluwademilade Nuga, Ryan O Dulay, Nikhil C. Patel, Truman Kula, Kozeta Libohova, Autumn Jackson-Butler, Wei‐Ling Tsou, Kristin Richardson, Sokol V. Todi

This paper develops a Drosophila model of DRPLA by expressing human ATN1 with normal or pathogenic polyglutamine repeats, showing that pathogenic ATN1 causes toxicity and identifies potential therapeutic targets.

Neurobiology of Disease · Feb 5, 2025Peer-reviewedNeuroscience