Author

Jeremy Y. Huang

Sanofi (France)ORCID 0000-0003-1433-4792Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Organism:mouse· 1 Assay:scRNA-seq· 1 Approach:statistical model· 1

Frequent Co-Authors

Anna S. Blazier· 1 shared Bailin ZhangiD· 1 shared Dimitry OfengeimiD· 1 shared Disha SoodiD· 1 shared Fabrizio PontarelliiD· 1 shared Fen HuangiD· 1 shared Giorgio GagliaiD· 1 shared Jennifer Hsiao‐NakamotoiD· 1 shared

Activity by Year

2024-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperNeuroscience

Anna S. Blazier

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1 paper

Recent·Most cited

Glial state changes and neuroinflammatory RIPK1 signaling are a key feature of ALS pathogenesis

Matija Zelic, Anna S. Blazier, Fabrizio Pontarelli, Michael J. LaMorte, Jeremy Y. Huang, Ozge E. Tasdemir-Yilmaz, Yi Ren, Sean K. Ryan, Pavithra Krishnaswami, Mikhail N. Levit, Disha Sood, Yao Chen, Joseph Gans, Xinyan Tang, Jennifer Hsiao‐Nakamoto, , Timothy R. Hammond

This study identifies glial state changes and RIPK1 signaling as key features of ALS pathogenesis, showing that blocking RIPK1 delays disease onset and modulates glial responses.

bioRxiv · Apr 12, 2024 · PreprintNeuroscience