Author

Wei Jun Gu

Columbia UniversityORCID 0000-0002-1480-2368Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

Wei Gu3 papers · Nanjing Normal University

Biology Disciplines

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Cell Biology· 1 Genetics· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Assay:DNA methylation· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Alan E. TomkinsoniD· 1 shared Albert H. KimiD· 1 shared Alberto M. PendásiD· 1 shared Alina VaitsiankovaiD· 1 shared Amanda Titus· 1 shared Andrea MusacchioiD· 1 shared Andrew Hwang· 1 shared Arianna Esposito-VerzaiD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 12 mutual co-author links

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1 shared paperGenetics

Alan E. TomkinsonORCID

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3 papers

Recent·Most cited

Cell BiologybioRxivPreprintAug 21, 2026

Set mediates chromosome alignment and Cohesin cleavage independently of direct PP2A-B56-binding in oocyte meiosis

Leonor Keating, Arianna Esposito-Verza, Warif El Yakoubi…·Katja Wassmann

This study shows Set is essential for chromosome alignment and Cohesin cleavage in oocyte meiosis, functioning through Aurora B regulation and chromatin environment modulation, independent of PP2A-B56 interaction.

DOI 10.64898/2026.08.20.745968

mouseDNA methylation

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NeuroscienceCell ReportsPeer-reviewedJan 23, 2025

The Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway

Hao Chen, Cole Ferguson, Dylan Charles Mitchell…·Albert H. Kim

This study shows that USP7 deletion in mice causes neurological phenotypes, including synaptic proteome changes and dendritic spine defects, independent of p53.

11 citationstop 3%

mouseexperimental assay

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GeneticsMolecular CellPeer-reviewedOct 1, 2024

Inactive Parp2 causes Tp53-dependent lethal anemia by blocking replication-associated nick ligation in erythroblasts

Xiaohui Lin, Dipika Gupta, Alina Vaitsiankova…·Shan Zha

The paper shows that inactive PARP2 causes Tp53-dependent lethal anemia by blocking replication-associated nick ligation in erythroblasts, explaining PARPi-induced hematological toxicities.

27 citationstop 5%

mouseDNA methylation

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