Author

Ke Qin

Nationwide Children's HospitalPrimary ORCID profile (0000-0001-7298-7826 · 1 paper)Unclaimed ORCID profile · follow to get notified of new preprints

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Same name, identified by ORCID

Ke QiniD1 paper · Scripps Research Institute

Biology Disciplines

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Molecular Biology· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Aaron VargheseiD· 1 shared Adithe RivaldiiD· 1 shared Albert M. IsaacsiD· 1 shared Alex Handler WagneriD· 1 shared Benjamin D. SunkeliD· 1 shared Benjamin KellyiD· 1 shared Cole A. HarringtoniD· 1 shared Delin MoiD· 1 shared

Activity by Year

2020-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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1 shared paperNeuroscience

Aaron VargheseORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

PEDIA-BRAIN: A single nuclei multiomic encyclopedia of the human pons provides a resource for normal development and disease vulnerability

Tianli Ding, Gary Schweickart, Kaitlin Kaiser, Adithe Rivaldi, Nicholas Marchal, Cole A. Harrington, Aaron Varghese, Ke Qin, Benjamin Kelly, Benjamin D. Sunkel, Kathryn Stahl, Jack D. Webb, Alex Handler Wagner, Jeffrey R. Leonard, Albert M. Isaacs, , Michelle Ariana Wedemeyer

PEDIA-BRAIN provides a single nuclei multiomic resource of the human pons across development, revealing oligodendrocyte maturation trajectories and disease-related perturbations in DMG and MS.

bioRxiv · Sep 21, 2025 · PreprintNeuroscience

Functional analysis of KIT gene structural mutations causing porcine dominant white phenotype by using genome edited mouse models

Guanjie Sun, Xinyu Liang, Ke Qin, Yufeng Qin, Xuan Shi, Peiqing Cong, Delin Mo, Xiaohong Liu, Yaosheng Chen, Zuyong He

The paper creates genome-edited mouse models to study KIT gene mutations in pigs and finds that only the combination of two structural mutations causes a dominant white phenotype.

Frontiers in Genetics · Mar 3, 2020Peer-reviewedMolecular Biology