Author

E. Hammer

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· 4

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Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Assay:proteomics· 3 Approach:genetic perturbation / CRISPR· 2 Organism:human· 2 Organism:mouse· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

F. Kliewe· 2 shared N. Endlich· 2 shared U. Voelker· 2 shared A. Gress· 1 shared A. Madsen· 1 shared A. Mirzaiebadizi· 1 shared A. T. Zech· 1 shared A. V. Busley· 1 shared

Activity by Year

2021-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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2 shared papersCell Biology

F. Kliewe

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Author profile →

4 papers

Recent·Most cited

Alternative splicing in mechanically stretched podocytes as a model of glomerular hypertension

F. Mattias, O. Tsoy, E. Hammer, A. Gress, S. Simm, C. T. Lio, S. Ameling, K. Amann, L. Dreher, U. Wenzel, T. Kacprowski, M. List, O. Kalinina, K. Endlich, J. Baumbach, , F. Kliewe

The paper investigates alternative splicing in mechanically stretched podocytes, identifying splicing events in Shroom3 and Myl6 that may contribute to hypertensive nephropathy.

bioRxiv · Jul 17, 2024Cell Biology

The tricellular junction protein ILDR2 in glomerulopathies: insights and implications

F. Siegerist, F. Kliewe, E. Hammer, P. Schakau, J. E. C. Soh, C. Weber, V. Puelles, M. Lindenmeyer, S. Reichelt-Wurm, V. Drenic, C. Chatziantoniou, C. Chadjichristos, Y. Zhang, M. Nauck, U. Völker, N. Endlich

This study investigates ILDR2's role in glomerulopathies, finding it upregulated in disease models and suggesting a protective effect against glomerular damage.

bioRxiv · May 3, 2024 · PreprintCell Biology

LZTR1 polymerization provokes cardiac pathology in recessive Noonan syndrome

A. V. Busley, O. Gutierrez-Gutierrez, E. Hammer, F. Koitka, A. Mirzaiebadizi, M. Steinegger, C. Pape, L. Boehmer, H. Schroeder, M. Kleinsorge, M. Engler, I. C. Cirstea, L. Gremer, D. Willbold, J. Altmueller, , L. Cyganek

This study identifies a novel LZTR1 variant causing cardiac hypertrophy by altering protein polymerization and ubiquitin ligase function, showing genetic correction can rescue the phenotype.

bioRxiv · Jan 10, 2023Cell Biology

ACTN2 mutant causes proteopathy in human iPSC-derived cardiomyocytes

A. T. Zech, M. Prondzynski, S. R. Singh, N. Pietsch, E. Orthey, E. Alizoti, J. Busch, A. Madsen, C. S. Behrens, M. Meyer-Jens, G. Mearini, M. D. Lemoine, E. Kraemer, D. Mosqueira, S. Virdi, , L. Carrier

This study shows that an ACTN2 mutation leads to proteopathy in human iPSC-derived cardiomyocytes through protein aggregation and activation of proteolytic systems.

bioRxiv · Oct 28, 2021Cell Biology