Author

S. Erschow

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

D. Hilfiker-Kleiner· 2 shared M. Ricke-Hoch· 2 shared M. Scherr· 2 shared S. Pietzsch· 2 shared A. Ganser· 1 shared A. Haase· 1 shared A. K. Bergmann· 1 shared B. Stapel· 1 shared

Activity by Year

2020-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersCancer Biology

D. Hilfiker-Kleiner

Mutual co-authors in cluster

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2 papers

Recent·Most cited

Targeted anti-BCR-ABL+ ALL therapy may benefit the heart

H. Kirchhoff, M. Ricke-Hoch, K. Wohlan, S. Pietzsch, U. Karsli, S. Erschow, R. Zweigerdt, A. Ganser, M. Eder, M. Scherr, D. Hilfiker-Kleiner

This paper shows that targeted therapies for BCR-ABL+ ALL can cause heart damage, but some treatments like dasatinib and venetoclax can reverse cardiac defects while others cannot.

bioRxiv · Jun 4, 2021 · PreprintCancer Biology

Increased prostaglandin-D2 in male but not female STAT3-deficient hearts shifts cardiac progenitor cells from endothelial to white adipocyte differentiation

E. Stelling, M. Ricke-Hoch, S. Erschow, S. Hoffman, A. K. Bergmann, M. Heimerl, S. Pietzsch, K. Battmer, A. Haase, B. Stapel, M. Scherr, O. Binah, J.-L. Balligand, D. Hilfiker-Kleiner

This study shows that male STAT3-deficient hearts have increased PGD2 secretion, leading to epigenetic changes in cardiac progenitor cells that shift their differentiation from endothelial to white adipocyte.

PLOS Biology · Dec 28, 2020Peer-reviewedCell Biology