Author

Jacob Waksmacki

University of Michigan

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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Approach:experimental assay· 3 Organism:human· 3 Organism:mouse· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Research Focus:database / resource· 1 Research Focus:differential expression· 1 Organism:Drosophila· 1

Frequent Co-Authors

Sami J. BarmadaiD· 4 shared Xingli LiiD· 4 shared Elizabeth M.H. TankiD· 3 shared Nicolás GómeziD· 3 shared Christopher H. Altheim· 2 shared Emile S. PinarbasiiD· 2 shared M. Rebecca GlineburgiD· 2 shared Megan M. DykstraiD· 2 shared

Activity by Year

2024-2025 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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4 shared papersNeuroscience

Sami J. BarmadaORCID

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Author profile →

4 papers

Recent·Most cited

Nemo-like kinase disrupts nuclear import and drives TDP43 mislocalization in ALS

Michael E. Bekier, Emile S. Pinarbasi, Gopinath Krishnan, Jack J. Mesojedec, Madelaine Hurley, Harisankar Harikumar Sheela, Catherine A. Collins, Layla Ghaffari, Martina de Majo, Erik M. Ullian, Mark Koontz, Sarah Coleman, Xingli Li, Elizabeth M.H. Tank, Jacob Waksmacki, , Sami J. Barmada

This study shows NLK disrupts nuclear import, causing TDP43 mislocalization in ALS, and suggests NLK as a therapeutic target.

Journal of Clinical Investigation · Jun 24, 2025Peer-reviewedNeuroscience

Stress granule formation helps to mitigate neurodegeneration

M. Rebecca Glineburg, Evrim Yildirim, Nicolás Gómez, Genesis Rodriguez, Jaclyn Pak, Xingli Li, Christopher H. Altheim, Jacob Waksmacki, Gerald M. McInerney, Sami J. Barmada, Peter K. Todd

This study investigates the role of stress granule formation in neurodegeneration, finding that reducing stress granules exacerbates disease phenotypes in models of ataxia, ALS, and FTD.

Nucleic Acids Research · Jul 17, 2024Peer-reviewedNeuroscience

TDP43 autoregulation gives rise to shortened isoforms that are tightly controlled by both transcriptional and post-translational mechanisms

Megan M. Dykstra, Kaitlin Weskamp, Nicolás Gómez, Jacob Waksmacki, Elizabeth M.H. Tank, M. Rebecca Glineburg, Allison G. Snyder, Emile S. Pinarbasi, Michael E. Bekier, Xingli Li, Jen Bai, Shameena Shahzad, Juno Nedumaran, Clare M. Wieland, Corey Stewart, , Sami J. Barmada

This study identifies TDP43 autoregulation as a source of shortened isoforms, showing they are regulated by NMD and post-translational degradation, and their dysregulation leads to neurodegeneration.

bioRxiv · Jul 2, 2024 · PreprintNeuroscience

Counter-regulation of RNA stability by UPF1 and TDP43

Nicolás Gómez, Caroline Hsieh, Xingli Li, Megan M. Dykstra, Jacob Waksmacki, Christopher H. Altheim, Yoel Bechar, Joseph R. Klim, Benjamin L. Zaepfel, Jeffrey D. Rothstein, Elizabeth M.H. Tank, Sami J. Barmada

The paper develops NMDq, a next-generation sequencing method to quantify NMD status, and applies it to ALS and FTD, finding no significant PTC differences but showing UPF1 regulates RNA homeostasis through alternative polyadenylation.

bioRxiv · Jan 31, 2024 · PreprintNeuroscience