Author

Caitrin Crudden

Vrije Universiteit AmsterdamORCID 0000-0002-7786-112XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Assay:proteomics· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

Martine J. SmitiD· 3 shared Carsten HoffmanniD· 2 shared Claudia V. Perez AlmeriaiD· 2 shared Julia DrubeiD· 2 shared Lotte Di NiroiD· 2 shared Marco H. SideriusiD· 2 shared Raimond HeukersiD· 2 shared An HendrixiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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3 shared papersBiochemistry

Martine J. SmitORCID

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Chemokine and opioid peptide scavenging through constitutive and ligand-induced release of ACKR3-bearing extracellular vesicles

Christie B. Palmer, Lucie Rospape, Max Meyrath, Caitrin Crudden, Manuel Counson, Anne‐Katrin Rohlfing, Lotte Di Niro, Ana Alonso Bartolomé, Cláudio Pinheiro, Vanessa Klapp, Ester Cassano, Stéphane A. Laporte, Stephen John Hill, Julia Drube, Carsten Hoffmann, , Andy Chevigné

This study shows ACKR3 is released on extracellular vesicles under both basal and ligand-induced conditions, sequestering chemokines and opioid peptides and modulating their signaling.

bioRxiv · Jun 19, 2026 · PreprintCell Biology

Constitutive activity of an atypical chemokine receptor revealed by inverse agonistic nanobodies

Claudia V. Perez Almeria, Omolade Otun, Roman R. Schlimgen, Thomas D Lamme, Lotte Di Niro, Caitrin Crudden, Jan Paul Bebelman, Noureldine Youssef, Lejla Musli, Shawn E. Jenjak, Vladimir Bobkov, Julia Drube, Carsten Hoffmann, Brian F. Volkman, Sébastien Granier, , Martine J. Smit

This study uses inverse agonistic nanobodies to reveal constitutive activity of ACKR3, showing it drives non-canonical signaling and basal cell motility, suggesting therapeutic potential.

Nature Communications · Dec 2, 2025Peer-reviewedBiochemistry

Disruption of basal CXCR4 oligomers impairs oncogenic properties in lymphoid neoplasms

Simon Mobach, Nick D. Bergkamp, Ziliang Ma, Marco Vincent Haselager, Stephanie Mareike Anbuhl, Daphne Jurriens, Jelle van den Bor, Ziming Wang, Caitrin Crudden, Jamie Lee Roos, Claudia V. Perez Almeria, Rick A. Boergonje, Martin J. Lohse, Reggie Bosma, Eric Eldering, , Raimond Heukers

This study shows that disrupting CXCR4 oligomers in lymphoid cancers reduces migration, survival signaling, and tumor growth, while sensitizing cells to venetoclax.

Proceedings of the National Academy of Sciences · Jun 11, 2025Peer-reviewedBiochemistry