Author

Mingee Chung

Emory 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· 4

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 4 Organism:human· 4 Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:gene regulatory network inference· 2 Assay:proteomics· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1

Frequent Co-Authors

Nicholas T. SeyfriediD· 4 shared Zachary T. McEachiniD· 4 shared Adam N. TrautwigiD· 3 shared Jonathan D. GlassiD· 3 shared Dennis W. DicksoniD· 2 shared Michael Emmerson WardiD· 2 shared Peter T. NelsoniD· 2 shared Ah Joung Rachel Yu· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 34 mutual co-author links

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4 shared papersNeuroscience

Nicholas T. SeyfriedORCID

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Author profile →

4 papers

Recent·Most cited

Temporal RNA splicing dysregulation in a human multicellular model of C9orf72 ALS

Berna Aliya, Shiqi Liu, Alison Mansfield, Solan Xiyuan Yao, Sabra Mouhi, Supriya S. Wariyar, Jesse Seth Tenkorang, Nuri E. Smith, Mingee Chung, Ah Joung Rachel Yu, Taylor Pio, Najah E.J. Smith, Sabrina H. Zhu, Adam N. Trautwig, Janani Parameswaran, , Jimena Andersen

This study uses human spinal cord organoids to model C9orf72 ALS, identifying early RNA splicing dysregulation and RBP network dysfunction as key features of the disease.

bioRxiv · Oct 14, 2026 · PreprintNeuroscience

TDP-43 dysfunction induces cryptic circular RNAs in ALS/FTD

Dario Dattilo, Flaminia Pellegrini, Simone Barattucci, Anna‐Leigh Brown, Jose Norberto S. Vargas, Ariana P. Gatt, Ryan D. Morrie, Georgiana Miller, Iris Bachmutsky, Zachary T. McEachin, Mingee Chung, Matthew J. Keuss, Eugeni M. Ryadnov, Matteo Zanovello, Puja R. Mehta, , Pietro Fratta

This study identifies TDP-43 dysfunction as a cause of cryptic circular RNA formation in ALS/FTD, showing their association with disease-relevant protein loss and potential as biomarkers.

bioRxiv · Sep 20, 2026 · PreprintNeuroscience

Molecular Subtyping Based on Hippocampal Cryptic Exon Burden Reveals Proteome-wide Changes Associated with TDP-43 Pathology across the Spectrum of LATE and Alzheimer's Disease

Adam N. Trautwig, Anantharaman Shantaraman, Mingee Chung, Eric B. Dammer, Lingyan Ping, Duc M. Duong, Leonard Petrucelli, Michael Emmerson Ward, Jonathan D. Glass, Peter T. Nelson, Allan I. Levey, Zachary T. McEachin, Nicholas T. Seyfried

This study identifies molecular subtypes based on cryptic exon burden in hippocampal tissue, revealing proteomic changes linked to TDP-43 pathology in LATE and Alzheimer's disease.

bioRxiv · May 30, 2025 · PreprintNeuroscience

TDP-43 toxic gain of function links ALS, FTD and Alzheimers Disease through splicing dysregulation

Welmoed van Zuiden, Thea Deborah Meimoun, Bar Chen, Aviad Siany, Bar Abarbanel, Lihi Moshe, Nancy‐Sarah Yacovzada, Emmanuel Amzallag, Aleksandar Rajkovic, Liat Alyagor, Eviatar Weizman, Manuela Neumann, Colin Smith, Karina McDade, Andrew Strange, , Eran Hornstein

This study identifies TDP-43-driven splicing dysregulation as a common mechanism in ALS, FTD, and Alzheimer's disease, linking them through mis-spliced mRNAs like APP.

bioRxiv · Apr 20, 2025 · PreprintNeuroscience