Vanessa Lundin

This study identifies how RNA splicing factor mutations drive myeloid neoplasm by disrupting proteomic networks through mis-splicing, validated via single-cell transcriptomics and proteomics.

This study shows that hemodynamic forces activate YAP signaling via Piezo1 in hemogenic endothelium, promoting HSC production by regulating metabolic and gene regulatory programs, while TAZ overactivation disrupts this balance.

This study identifies UBA1 mis-splicing as a therapeutic target in SF3B1-mutant myelodysplastic syndromes, showing that UBA1 inhibition sensitizes these cells to treatment.

The paper identifies ZCCHC6 and DIS3L2 as key regulators of RNA decay during terminal erythropoiesis, showing their role in post-transcriptional globin switching and {gamma}-globin stabilization.