Author

Jincheng Gao

Institut für Kardiovaskuläre Physiologie und PathophysiologieORCID 0000-0002-5618-0755Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Physiology· 2 Neuroscience· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 3 Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Organism:zebrafish· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1

Frequent Co-Authors

Almke BaderiD· 3 shared Barbara WalzogiD· 3 shared Daniela BegandtiD· 3 shared Annette Zehrer· 2 shared Bettina SchmidiD· 2 shared Mathis RichteriD· 2 shared Oliver SoehnleiniD· 2 shared Xiang Wei· 2 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersPhysiology

Almke BaderORCID

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3 papers

Recent·Most cited

PhysiologyCell Death and DiseasePeer-reviewedJan 12, 2026

Mutations in VPS18 lead to a neutrophil maturation defect associated with disturbed vesicle homeostasis

Jincheng Gao, Almke Bader, Monika I. Linder…·Daniela Begandt

This study shows that VPS18 mutations disrupt neutrophil maturation by impairing vesicle dynamics and autophagy, leading to neutropenia and recurrent infections.

DOI 10.1038/s41419-025-08338-w

humanmouse

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PhysiologyJournal of Leukocyte BiologyPeer-reviewedOct 31, 2025

SCAMP3 is essential for proper formation and function of neutrophil granules

Almke Bader, Jincheng Gao, Nina Reiter…·Daniela Begandt

The paper shows SCAMP3 is essential for neutrophil granule formation and function, with Scamp3-deficient neutrophils showing impaired bacterial killing in vitro.

DOI 10.1093/jleuko/qiaf153

mousezebrafish

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NeurosciencebioRxivPreprintSep 19, 2025

The nuclear receptor NR4A1 serves as a neutrophil-intrinsic regulator mitigating stroke severity

Jan‐Kolja Strecker, Yannick Schmidt, Marie Liebmann…·Jens Minnerup

This study identifies NR4A1 as a neutrophil-intrinsic regulator that reduces stroke severity by limiting inflammation and brain damage through pharmacological modulation.

1 citation

humanmouse

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