Author

Agnes Ulfig

University of IcelandORCID 0000-0003-2689-6311Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetics· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2

Frequent Co-Authors

Hans Tomas BjornssoniD· 2 shared Jill A. FahrneriD· 2 shared Sara Tholl HalldorsdottiriD· 2 shared Ellen Dagmar BjörnsdóttiriD· 1 shared Hilmar Orn Gunnlaugsson· 1 shared Meghna VinodiD· 1 shared Romain Maurice Jacques LasseuriD· 1 shared Stefán PéturssoniD· 1 shared

Activity by Year

2026-2026 · peak 2/yr

Co-Author Collaboration Network

9 top collaborators · 31 mutual co-author links

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2 shared papersMolecular Biology

Hans Tomas BjornssonORCID

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2 papers

Recent·Most cited

Molecular BiologybioRxivPreprintOct 10, 2026

Loss of KMT2D accelerates hypertrophic chondrocyte differentiation and senescence by increasing mitochondrial ROS production

Sara Tholl Halldorsdottir, Stefán Pétursson, Jill A. Fahrner…·Hans Tomas Bjornsson

This study shows that KMT2D deficiency causes chondrocyte hypertrophy and senescence via increased mitochondrial ROS, leading to skeletal abnormalities in KS1.

DOI 10.64898/2026.03.18.712470

mouseexperimental assay

𝕏 PostBluesky

GeneticsDisease Models & MechanismsPeer-reviewedSep 9, 2026

A patient derived missense mouse model of Kabuki syndrome 1

Sara Tholl Halldorsdottir, Meghna Vinod, Hilmar Orn Gunnlaugsson…·Hans Tomas Bjornsson

The paper introduces a missense mouse model of Kabuki syndrome with intact KMT2D function, showing similar phenotypes to loss-of-function models but without altered adult neurogenesis and with novel kidney agenesis.

DOI 10.1242/dmm.052775

mouseexperimental assay

𝕏 PostBluesky