Author

M. Scheller

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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Cancer Biology· 1 Immunology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:differential expression· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

A. Solomon· 2 shared L. Shlush· 2 shared N. Kaushansky· 2 shared A. Bercovich· 1 shared A. Debes· 1 shared A. M. Zeiher· 1 shared B. Schuhmacher· 1 shared C. Mueller-Tidow· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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2 shared papersImmunology

A. Solomon

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Monocyte-derived microglia with Dnmt3a mutation cause motor pathology in aging mice

J.-S. Kim, S. Trzebanski, S.-H. Shin, N. C. Ilani, N. Kaushansky, M. Scheller, A. Solomon, Z. Liu, O. Aust, S. Boura-Halfon, L. Amann, M. Prinz, F. Ginhoux, R. Avraham, C. Mueller-Tidow, , S. Jung

This study shows that monocyte-derived microglia with a Dnmt3a mutation cause motor deficits in aging mice, resembling Parkinsonian disorders.

bioRxiv · Nov 16, 2023Immunology

DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts

M. Shumliakivska, G. Luxan, I. Hemmerling, W. T. Abplanalp, X. Li, M. Scheller, C. Muller-Tidow, F. Leuschner, B. Schuhmacher, A. Debes, S.-F. Glaser, M. Muhly Reinholz, K. Kirschbaum, J. Hoffmann, E. Nagel, , S. Dimmeler

This study shows that DNMT3A mutations in hematopoietic cells drive cardiac fibrosis by activating fibroblasts through paracrine signaling, contributing to heart failure progression.

bioRxiv · Jan 7, 2023Physiology

Inflammatory signals from fatty bone marrow supports the early stages of DNMT3a driven clonal hematopoiesis

N. Zioni, A. Bercovich, N. Chapal-Ilani, A. Solomon, E. Petrovich, M. .Sacma, H. Geiger, M. Scheller, C. Müller-Tidow, D. Lipka, E. Shlush, M. Minden, N. Kaushansky, L. Shlush

This study shows that fatty bone marrow (FBM) promotes DNMT3A-driven clonal hematopoiesis by enhancing inflammatory signals like IL-6, which can be inhibited by blocking the IL-6 receptor.

bioRxiv · Jan 13, 2022Cancer Biology