Author

Jochen Seebach

University of Münster

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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Cell Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:development & morphogenesis· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

Hans‐Joachim SchnittleriD· 2 shared Jan Philip KipckeiD· 2 shared Jonas FranziD· 2 shared Maria Odenthal-SchnittleriD· 2 shared Vesna Bojovic· 2 shared Erez RaziD· 1 shared Franziska Merten· 1 shared Johannes Andreas EbleiD· 1 shared

Activity by Year

2025-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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2 shared papersImmunology

Hans‐Joachim SchnittlerORCID

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2 papers

Recent·Most cited

TNF-a induces VE-cadherin-dependent gap/JAIL cycling through an intermediate state essential for neutrophil transmigration

Jan Philip Kipcke, Maria Odenthal-Schnittler, Mohammed Aldirawi, Jonas Franz, Vesna Bojovic, Jochen Seebach, Hans‐Joachim Schnittler

This study shows TNF-α induces an inflammatory morphological phenotype (IMP) through VE-cadherin-dependent gap/JAIL cycling, essential for neutrophil transmigration.

Frontiers in Immunology · Sep 9, 2025Peer-reviewedImmunology

A critical role for VE-cadherin in regulating actin dynamics during endothelial maturation and non-inflammatory activation via a tension-sensitive intermediate state

Jonas Franz, Maria Odenthal-Schnittler, Jan Philip Kipcke, Jochen Seebach, Zahra Labbaf, Franziska Merten, Vesna Bojovic, Johannes Andreas Eble, Erez Raz, Milos Galic, Hans‐Joachim Schnittler

The paper identifies a tension-sensitive intermediate state in endothelial cells during non-inflammatory activation, which regulates actin dynamics and barrier function through VE-cadherin and MLC-dephosphorylation.

bioRxiv · Aug 5, 2025 · PreprintCell Biology