Author

S. Kallabis

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· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell type annotation· 2 Research Focus:chromatin & epigenetic regulation· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1

Frequent Co-Authors

A. Das· 1 shared A. Demczuk· 1 shared A. Kaczmarek· 1 shared A. Lofrano· 1 shared A. Sen· 1 shared B. S. Franklin· 1 shared D. Bertheloot· 1 shared D. Pla-Martin· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 13 mutual co-author links

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1 shared paperCell Biology

A. Das

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

ERLIN1/2 scaffolds bridge TMUB1 and RNF170 and restrict cholesterol esterification to regulate the secretory pathway

M. Veronese, S. Kallabis, A. Kaczmarek, L. Robers, S. Schumacher, A. Das, A. Lofrano, S. Brodesser, S. Müller, K. Hofmann, M. Krüger, E. I. Rugarli

This study identifies ERLIN1/2 scaffolds that mediate TMUB1-RNF170 interactions, regulate cholesterol esterification, and maintain ER cholesterol levels to control Golgi morphology and the secretory pathway.

bioRxiv · Jan 17, 2024Cell Biology

Platelet-derived transcription factors license human monocyte 1 inflammation

I. Hawwari, N. Rosero, S. Maasewerd, M. Jentzsch, A. Demczuk, L. S. Ribeiro, L. S. Teichmann, L. Meffert, S. Kallabis, F. Meissner, M. Noval Rivas, M. A. Arditi, D. Bertheloot, B. S. Franklin

This study shows platelets are crucial for human monocyte inflammation, as their absence causes immunoparalysis and their addition restores cytokine responses.

bioRxiv · Aug 10, 2022Immunology

Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA

D. Pla-Martin, A. Sen, S. Kallabis, J. Nuechel, K. Maliphol, J. Hofmann, M. Krueger, R. J. Wiesner

The paper identifies a mechanism involving Twinkle, ATAD3, SAMM50, and VPS35 that selectively removes mutant mtDNA through autophagy, offering therapeutic potential for mtDNA diseases and aging.

bioRxiv · Aug 6, 2021 · PreprintCell Biology