Author

S. Capellmann

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

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:mouse· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

M. Huber· 3 shared M. Arock· 2 shared M. Kauffmann· 2 shared B. Tirosh· 1 shared C. Liedtke· 1 shared C. Martin· 1 shared F. Levi-Schaffer· 1 shared G. Bronneberg· 1 shared

Activity by Year

2023-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 28 mutual co-author links

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3 shared papersImmunology

M. Huber

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Author profile →

3 papers

Recent·Most cited

KIRA6 is an effective and versatile mast cell inhibitor of IgE-mediated activation

T. Wilhelm, V. Wunderle, S. Boukeileh, J. Gossen, M. A. Margreiter, R. Sakurov, S. Capellmann, M. Schwoerer, N. Ahmed, G. Bronneberg, M. Arock, C. Martin, T. Schubert, F. Levi-Schaffer, G. Rossetti, , M. Huber

This study identifies KIRA6 as a dual inhibitor of LYN and FYN that suppresses IgE-mediated mast cell activation and inflammation.

bioRxiv · Apr 18, 2024Immunology

SR-BI regulates the synergistic mast cell response by modulating the plasma membrane-associated cholesterol pool

S. Capellmann, M. Kauffmann, M. Arock, M. Huber

This paper identifies SR-BI as a regulator of mast cell activation by modulating plasma membrane cholesterol, affecting synergistic responses to multiple stimuli.

bioRxiv · Jun 21, 2023Immunology

Transformation of primary murine peritoneal mast cells by constitutive KIT activation as a result of lost Cdkn2a/Arf expression

S. Capellmann, R. Sonntag, H. Schueler, S. K. Meurer, L. Gan, M. Kauffmann, K. Horn, H. Koenigs-Werner, R. Weiskirchen, C. Liedtke, M. Huber

The paper describes the generation of a transformed murine mast cell line, PMC-306, and identifies the loss of Cdkn2a/Arf as the cause of its immortalization.

bioRxiv · Jan 24, 2023 · PreprintImmunology