Author

Xaver Koenig

Medical University of ViennaORCID 0000-0002-2423-4966Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Pharmacology & Toxicology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Assay:electronic health records· 1 Assay:electrophysiology· 1

Frequent Co-Authors

Anna Stary‐WeinzingeriD· 1 shared Attila KissiD· 1 shared Bruno Karl PodesseriD· 1 shared Christopher DostaliD· 1 shared Elena LilliuiD· 1 shared Gaetan LopeziD· 1 shared Hannes TodtiD· 1 shared Helmut KubistaiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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1 shared paperPharmacology & Toxicology

Anna Stary‐WeinzingerORCID

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2 papers

Recent·Most cited

PhysiologybioRxivPreprintOct 4, 2026

CONSTITUTIVE STIM1L DELETION ALTERS STORE-OPERATED CALCIUM ENTRY KINETICS BUT DOES NOT PERTURB THE DEVELOPMENT AND FUNCTION OF MOUSE SKELETAL MUSCLE

Olivier Dopont, Gaetan Lopez, Elena Lilliu…·Stéphane Koenig

This study shows that constitutive STIM1L deletion in mice alters SOCE activation kinetics in myotubes but does not affect skeletal muscle development or function.

DOI 10.64898/2026.09.28.755229

mouseelectronic health records

𝕏 PostBluesky

Pharmacology & ToxicologyAmerican Journal of Physiology-Heart and Circulatory PhysiologyPeer-reviewedAug 13, 2025

The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac Nav1.5 channels

Jakob Sauer, Jessica Marksteiner, Martin HOHENEGGER…·Oliver Kudlacek

This study shows empagliflozin enhances peak sodium current in Nav1.5 channels by acting as a pharmacological chaperone, potentially reducing arrhythmia risk in Duchenne muscular dystrophy.

4 citations

mouserat

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