Sandra Schrenk

This study identifies a PI3K-RAC1 signaling axis that promotes endothelial dysfunction in TIE2-mutated venous malformations by enhancing migration and vascular lumen size.

This study creates a TIE2-L914F mouse model to study venous malformation progression and shows it responds to rapamycin treatment.

This study shows that mosaic expression of the TIE2 p.L914F mutation during mouse development causes partial embryonic lethality and venous malformation.

This study shows that the TIE2 p.L914F mutation causes embryonic lethality and vascular defects in mice, highlighting its incompatibility with early vascular development.

This study shows that TIE2-mutant endothelial cells overexpress Semaphorin 3A and 3F, which repel wild-type endothelial cells and drive pathological lumen expansion in venous malformations.