Michiel Vanhooydonck

This study evaluates a COL1A2 variant of uncertain significance using zebrafish knock-in models, showing that pathogenic variants cause skeletal abnormalities while VUS and benign variants do not.

This study compares CRISPR-mediated homology-directed repair (HDR) and prime editing (PE) for precise genetic variant knock-in in zebrafish, finding PE achieves higher editing efficiency and fewer off-target effects.

This study identifies ZFHX4 loss-of-function variants as a cause of a neurodevelopmental disorder with distinctive facial features and brain abnormalities, supported by zebrafish models.

This study develops a zebrafish model of thoracic aortic dissection and rupture by knocking out SMAD3 and SMAD6 genes, revealing novel pathways and potential therapeutic targets.

This study shows that loss of atp6v1e1b in zebrafish causes multisystemic defects linked to reduced organelle acidification, revealing new biological impacts of v-ATPase dysfunction.