Author

Katrina Meyer

Max Delbrück CenterORCID 0000-0002-8244-6887Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:cell-cell communication· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Approach:statistical model· 1

Frequent Co-Authors

Matthias SelbachiD· 2 shared Altuna AkaliniD· 1 shared Bora UyariD· 1 shared Duncan S. SutherlandiD· 1 shared Ina‐Maria RudolphiD· 1 shared Jemila P. GomesiD· 1 shared Johan PalmfeldtiD· 1 shared Koshi ImamiiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersNeuroscience

Matthias SelbachORCID

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2 papers

Recent·Most cited

Familial Alzheimer disease mutation identifies novel role of SORLA in release of neurotrophic exosomes

Kristian Juul‐Madsen, Ina‐Maria Rudolph, Jemila P. Gomes, Katrina Meyer, Peter Lund Ovesen, Malgorzata J. Górniak-Walas, Marianna Kokoli, Narasimha Swamy Telugu, Malthe von Tangen Sivertsen, Duncan S. Sutherland, Johan Palmfeldt, Sebastian Diecke, Olav M. Andersen, Matthias Selbach, Thomas E. Willnow

This study identifies a novel role for SORLA in regulating exosome release and neurotrophic function, linking SORL1 mutations to Alzheimer's disease pathology.

bioRxiv · Apr 22, 2025 · PreprintNeuroscience

Pathogenic mutations of human phosphorylation sites affect protein-protein interactions

Trëndelina Rrustemi, Katrina Meyer, Yvette Roske, Bora Uyar, Altuna Akalin, Koshi Imami, Yasushi Ishihama, Oliver Daumke, Matthias Selbach

The paper investigates how pathogenic mutations at phosphorylation sites affect protein-protein interactions, showing that such mutations disrupt phosphorylation-dependent motifs and alter cellular functions.

Nature Communications · Apr 11, 2024Peer-reviewedSystems Biology