Author

Madeline J. Caduc

RWTH Aachen UniversityORCID 0000-0001-9880-4709Unclaimed 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 signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

Gerhard Müller‐NeweniD· 2 shared Marcelo A. S. ToledoiD· 2 shared Steffen KoschmiederiD· 2 shared Andrea Küster· 1 shared Bärbel Junge· 1 shared Cristina Baquero López· 1 shared Dickson W.L. WongiD· 1 shared Eva Miriam BuhliD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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2 shared papersCancer Biology

Gerhard Müller‐NewenORCID

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2 papers

Recent·Most cited

Cancer BiologybioRxivPreprintOct 10, 2025

The V617F mutation in JAK2 renders myeloid cells more sensitive to IL-6-mediated gp130 signaling

Henning Schurse, Marcelo A. S. Toledo, Andrea Küster…·Gerhard Müller‐Newen

This study shows that the JAK2 V617F mutation enhances IL-6 sensitivity by promoting gp130 dimerization and expression in myeloid cells, contributing to chronic inflammation in MPN.

DOI 10.1101/2025.10.10.681590

humanproteomics

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Cancer BiologybioRxivPreprintDec 23, 2024

Inhibition of JAK2V617F-Driven Neoplastic Endothelial Dysfunction by IFNα as a Novel Antifibrotic Mechanism

Madeline J. Caduc, Mohamed H. Elsafi Mabrouk, Martin Graßhoff…·Marcelo A. S. Toledo

This study identifies JAK2V617F zygosity-specific vascular changes in MPN and shows IFNα inhibits EndMT, offering a novel antifibrotic mechanism.

1 citation

mousescRNA-seq

𝕏 PostBluesky