Author

Haoyu Chi

University College LondonORCID 0009-0008-8954-6240Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:differential expression· 1 Assay:metabolomics· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

Chih-Yao ChungiD· 2 shared Michael R. DucheniD· 2 shared Preethi SheshadriiD· 2 shared Anitta R. ChackoiD· 1 shared Benjamin O’CallaghaniD· 1 shared David L. SelwoodiD· 1 shared Diana PendiniD· 1 shared Fleur VansenneiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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2 shared papersNeuroscience

Chih-Yao ChungORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

NeuroscienceNature CommunicationsPeer-reviewedMay 26, 2026

Pathogenic variants in autophagy-tethering factor EPG5 drive neurodegeneration through mitochondrial dysfunction and innate immune activation

Kritarth Singh, Hormos Salimi Dafsari, Olivia Gillham…·Michael R. Duchen

This study identifies EPG5 mutations causing neurodegeneration via mitochondrial dysfunction and innate immune activation in patient-derived cells.

4 citationstop 2%

humanbulk RNA-seq

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Cell BiologyStem Cell ReportsPeer-reviewedMar 13, 2025

Metabolic remodelling in hiPSC-derived myofibres carrying the m.3243A>G mutation

Gabriel E. Valdebenito, Anitta R. Chacko, Chih-Yao Chung…·Michael R. Duchen

This study generates hiPSC-derived myofibres with the m.3243A>G mutation to model mitochondrial disease, showing metabolic and physiological changes related to mutation load.

3 citations

humanproteomics

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