Author

Wei Shen

ARUP Laboratories;

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Same name, identified by ORCID

Biology Disciplines

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Neuroscience· 2 Developmental Biology· 1

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

ALEKSANDAR BAJIC· 1 shared ALEX SHCHEGLOVITOV· 1 shared Andong ZhangiD· 1 shared ANDREW HARRAHILL· 1 shared ANTHONY S. RICCIARDULLI· 1 shared Catherine Pan· 1 shared COLIN MAGUIRE· 1 shared ERIN B. TAYLOR· 1 shared

Activity by Year

2024-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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1 shared paperNeuroscience

ALEKSANDAR BAJIC

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

MAST1 is neuron-specific regulator of mitochondrial trafficking and abundance in human brain tissue

H M Arif Ullah, KANDY L. NAPAN, IVAN KHIMACH, MIGUEL A. CUEVAS, YONGSOO KIM, ERIN B. TAYLOR, MARIA A. SERRANO, ANTHONY S. RICCIARDULLI, SOPHIA ANDREADIS, ZHENNI JIN, NICOLE LOSURDO, ANDREW HARRAHILL, COLIN MAGUIRE, JEAN J. KIM, ALEKSANDAR BAJIC, , ALEX SHCHEGLOVITOV

This study identifies MAST1 as a neuron-specific regulator of mitochondrial trafficking and abundance, linking its mutations to neuronal mitochondrial dysfunction and microcephaly.

bioRxiv · Nov 5, 2026 · PreprintNeuroscience

Cross-Tissue Inflammatory Convergence Supports a Putative Muscle-Brain Axis in Alzheimer's Disease

Andong Zhang, Wei Shen, Shijun Yan, Jing Chen, Xiaoyan Liu, Jingfeng Zou, Shaotian Li, Shanshan Hu, Yiting Liu, Catherine Pan, Zhuoqing Lan, Guoping Peng, Qin Zhang, Wen Peng, Fariba Ahmadizar, , the Alzheimer’s Disease Neuroimaging Initiative

The paper identifies shared inflammatory pathways between aging skeletal muscle and Alzheimer's disease brain tissue, detectable in peripheral blood, and prioritizes candidate regulators.

bioRxiv · Oct 8, 2026 · PreprintNeuroscience

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Shuo Chao, Jun Lu, Lijun Li, Hongyan Guo, Kuipeng Xu, Ning Wang, Shu‐Xian Zhao, Xiao-Wen Jin, Shao-Ge Wang, Shen Yin, Wei Shen, Minghui Zhao, Gui‐An Huang, Qing‐Yuan Sun, Zhao‐Jia Ge

This study shows maternal obesity causes oocyte genome hyper-methylation via increased DNMTs, which can be partially transmitted to F2 offspring, and melatonin reduces this hyper-methylation through the cAMP/PKA/CREB pathway.

eLife · Dec 6, 2024Peer-reviewedDevelopmental Biology