Author

T. Poth

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 Physiology· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1

Frequent Co-Authors

M. Breinig· 2 shared P. Schirmacher· 2 shared A. Fischer· 1 shared A. Lomakin· 1 shared A. Maida· 1 shared A. Mhamane· 1 shared A. Weider· 1 shared A. Zeigerer· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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2 shared papersCancer Biology

M. Breinig

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Author profile →

3 papers

Recent·Most cited

Integrated combinatorial functional genomics and spatial transcriptomics of tumors decodes genotype to phenotype relationships

M. Breinig, A. Lomakin, E. Heidari, M. Ritter, G. Rukhovich, L. Boese, L. Butthof, L. Wendler-Link, H. Wiethoff, T. Poth, F. Sahm, P. Schirmacher, O. Stegle, M. Gerstung, D. Tschaharganeh

The paper introduces CHOCOLAT-G2P, a method integrating functional genomics and spatial transcriptomics to study genotype-phenotype relationships in tumors, revealing zonation patterns and epistasis in liver cancer.

bioRxiv · May 14, 2024 · PreprintCancer Biology

Phosphatidylinositol 4-kinase III alpha governs cytoskeletal organization for invasiveness of liver cancer cells

C. S. Tran, J. Kersten, M. Breinig, J. Yan, T. Poth, O. Colasanti, T. Riedl, S. Faure-Dupuy, S. Diehl, L. Verhoye, T.-F. Li, M. Lingemann, P. Schult, G. Ahlen, L. Frelin, , V. Lohmann

This study identifies PI4KIII's role in promoting liver cancer invasiveness through cytoskeletal reorganization via PIK3C2γ and Akt2/paxillin-cofilin signaling.

bioRxiv · May 22, 2023Cell Biology

Hepatocyte-specific activity of TSC22D4 triggers progressive NAFLD by impairing mitochondrial function

G. Wolff, M. Sakurai, A. Mhamane, A. Maida, I. K. Deligiannis, K. Yin, P. Weber, A. Weider, M. Troullinaki, A. Zeigerer, M. Roden, N. Volk, T. Poth, T. Hackert, L. Wiedmann, , S. Herzig

This study shows that deleting TSC22D4 in hepatocytes reduces liver damage in NASH by improving mitochondrial function and lipid metabolism.

bioRxiv · Dec 17, 2021Physiology