Author

Peter Andreas Matthiessen

Johannes Gutenberg University MainzORCID 0009-0008-6630-3799Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 1 Genetics· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Assay:proteomics· 2 Approach:statistical model· 2 Research Focus:cell-cell communication· 1 Research Focus:drug response / drug discovery· 1 Organism:human· 1

Frequent Co-Authors

Helen May‐SimeraiD· 2 shared Bernhard SchermeriD· 1 shared Christina Klausen· 1 shared Dagmar WachteniD· 1 shared Emeline F. NandrotiD· 1 shared Emilia KieckhöferiD· 1 shared Gunnar Glaßer· 1 shared Ingo LieberwirthiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersCell Biology

Helen May‐SimeraORCID

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2 papers

Recent·Most cited

Cell BiologybioRxivPreprintOct 16, 2025

Loss of ciliary proteins IFT20 and IFT88 results in defective phagocytosis and metabolism in the RPE

Peter Andreas Matthiessen, Lotta Elisabeth Wagner, Karsten Boldt…·Helen May‐Simera

The paper shows that loss of IFT20 and IFT88 in RPE cells impairs phagocytosis and metabolism by affecting photoreceptor binding, membrane morphology, and mitochondrial function.

DOI 10.1101/2025.10.16.682843

humanproteomics

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GeneticsbioRxivPreprintMar 7, 2024

Loss of Bbs8 leads to cystic kidney disease in mice with reduced acetylation of ciliary alpha-tubulin through HDAC2

Emilia Kieckhöfer, Julia Günzler, Peter Andreas Matthiessen…·Bernhard Schermer

This study shows that loss of Bbs8 in mice causes cystic kidney disease by reducing ciliary alpha-tubulin acetylation through increased HDAC2 activity.

DOI 10.1101/2024.03.07.583949

mouseproteomics

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