Author

Timon E. Adolph

Innsbruck Medical University

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

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Molecular Biology· 2

Signature Assays, Organisms & Methods

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Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Approach:deep learning· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Assay:proteomics· 1

Frequent Co-Authors

Ahmed Nabil HegazyiD· 1 shared Alexander ScheffoldiD· 1 shared Andreas DiefenbachiD· 1 shared Andreas Radbruch· 1 shared Andreas WinteriD· 1 shared Anja A. Kühl· 1 shared Anja Andrea KühliD· 1 shared Antigoni TriantafyllopoulouiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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1 shared paperMolecular Biology

Ahmed Nabil HegazyORCID

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2 papers

Recent·Most cited

IBDome: An integrated molecular, histopathological, and clinical atlas of inflammatory bowel diseases

Christina Plattner, Gregor Sturm, Anja Andrea Kühl, Raja Narayana Atreya, Sandro Carollo, Dietmar Rieder, Raphael Gronauer, Michael Günther, Steffen Ormanns, Claudia Manzl, Stefan Wirtz, Asier Rabasco Meneghetti, Ahmed Nabil Hegazy, Jay V. Patankar, Zunamys Itzell Carrero, , Jakob Nikolas Kather

This study integrates multi-omic and multimodal data from IBD patients to identify molecular, histopathological, and clinical features associated with inflammatory bowel diseases.

Gastroenterology · Mar 27, 2025Peer-reviewedMolecular Biology

Mitochondrial cardiolipin metabolism controlled by tafazzin enables ferroptosis

Yvonne Wohlfarter, Judith Hagenbuchner, Utku Horzum, Gregor Oemer, Andreas Winter, Markus Seifert, Julian Schwärzler, Janik Kokot, Pablo Hernansanz‐Agustín, Viktorija Jurić, Luiz Felipe Garcia Suoza, Heribert Talasz, José Antonio Enríquez Domínguez, Hesso Farhan, Timon E. Adolph, , Markus Andreas Keller

The paper shows that tafazzin deficiency in Barth Syndrome protects against ferroptosis by altering mitochondrial cardiolipin metabolism, affecting VDAC function and reducing ROS availability for ferroptosis.

bioRxiv · Oct 25, 2024 · PreprintMolecular Biology