Author

Viktorija Jurić

Innsbruck Medical UniversityORCID 0000-0003-2916-9080Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:clustering· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1 Approach:machine learning (classical)· 1

Frequent Co-Authors

Markus Andreas KelleriD· 3 shared Janik KokotiD· 2 shared Johannes ZschockeiD· 2 shared Andreas WinteriD· 1 shared Daniela KaralliD· 1 shared Denise KummeriD· 1 shared Fabian DorningeriD· 1 shared Georg Golderer· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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3 shared papersBiochemistry

Markus Andreas KellerORCID

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3 papers

Recent·Most cited

BiochemistryBiochimiePeer-reviewedAug 1, 2026

Beyond the surface: plasmalogens are dispensable for retinal integrity and fertility in the mouse

Ilaria Dorigatti, Viktorija Jurić, Michael J.F. Blumer…·Katrin Watschinger

This study compares Gnpat and Peds1 knockout mice to determine the role of plasmalogens in retinal integrity and fertility, finding that plasmanyl lipids can compensate for plasmalogen loss.

1 citation

mouseexperimental assay

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BiochemistrybioRxivPreprintJul 22, 2025

Biochemical signatures from dried blood spots in untargeted metabolics are influenced by matrix effects

Jan-Clemens Cremer, Viktorija Jurić, Jakob M. Koch…·Markus Andreas Keller

The paper investigates matrix effects on metabolite recovery from dried blood spots (DBS) and shows that despite these effects, DBS can be used for diagnostics with proper validation.

DOI 10.1101/2025.07.22.666056

humanmetabolomics

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Molecular BiologybioRxivPreprintOct 25, 2024

Mitochondrial cardiolipin metabolism controlled by tafazzin enables ferroptosis

Yvonne Wohlfarter, Judith Hagenbuchner, Utku Horzum…·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.

1 citation

human

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