Author

Jiechao Zhou

Johns Hopkins UniversityORCID 0000-0002-7879-0757Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 4 Research Focus:differential expression· 3 Organism:mouse· 3 Assay:proteomics· 3 Research Focus:cell type annotation· 2 Organism:human· 2 Research Focus:protein structure prediction· 2 Research Focus:cell-cell communication· 1

Frequent Co-Authors

Paul F. WorleyiD· 4 shared Wenchi ZhangiD· 2 shared Alexander H. Barrett· 1 shared Alexander J. Platero· 1 shared Alfredo KirkwoodiD· 1 shared Binhui ZhaoiD· 1 shared Borislav DejanoviciD· 1 shared Daniel SeveríniD· 1 shared

Activity by Year

2021-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 17 mutual co-author links

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4 shared papersNeuroscience

Paul F. WorleyORCID

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4 papers

Recent·Most cited

TRIM32-UBQLN2-p62 axis promotes TDP-43 inclusion formation and amyloid aggregation through shuttle condensates

Ziyan He, Jiechao Zhou, Rongzhen Zhang, Fei Meng, David W. Nauen, Juan Carlos Troncoso, Paul F. Worley, Wenchi Zhang

This study identifies a molecular pathway involving TRIM32, UBQLN2, and p62 that forms condensates promoting TDP-43 aggregation in neurodegenerative diseases.

bioRxiv · Feb 14, 2026 · PreprintNeuroscience

An autophagy adaptor TRIAD3A promotes tau fibrillation by phase separation

Jiechao Zhou, Yang ‘an Chuang, Javier Redding-Ochoa, Alexander J. Platero, Alexander H. Barrett, Juan C. Troncoso, Paul F. Worley, Wenchi Zhang

This study identifies TRIAD3A as an autophagy adaptor that promotes tau fibrillation through phase separation and ubiquitination.

Alzheimer s & Dementia · Dec 1, 2024Peer-reviewedNeuroscience

Neuronal pentraxin Nptx2 regulates complement activity in the brain

Jiechao Zhou, Sarah D. Wade, David R. Graykowski, Mei-Fang Xiao, Binhui Zhao, Lucia AA Giannini, Jesse E. Hanson, John Cornelis Van Swieten, Morgan Sheng, Paul F. Worley, Borislav Dejanovic

This study identifies Nptx2 as a regulator of complement activity in the brain, showing its role in preventing microglial synapse elimination in health and disease.

Science Translational Medicine · Mar 29, 2023Peer-reviewedNeuroscience

All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

Daniel Severín, Su Z. Hong, Seung‐Eon Roh, Shiyong Huang, Jiechao Zhou, Michelle Bridi, Ingie Hong, Sachiko Murase, Sarah Robertson, Rebecca P. Haberman, Richard L. Huganir, Michela Gallagher, Elizabeth M. Quinlan, Paul F. Worley, Alfredo Kirkwood

The paper shows that monocular deprivation in mouse visual cortex causes an all-or-none elimination of pyramidal cell connections to parvalbumin-positive interneurons, which is necessary for ocular dominance plasticity.

Proceedings of the National Academy of Sciences · Sep 10, 2021Peer-reviewedNeuroscience