Ralitsa Radostinova Madsen

This study shows that mTOR signalling, not clock gene rhythms, drives daily physiological variations in mammals and plants.

This study shows that PIK3CA mutations cause lineage-specific niche changes in vascular endothelium, leading to tissue malformations that can be partially prevented by PI3K inhibition.

The paper develops zebrafish models of PROS to show that PIK3CA mutations cause non-cell-autonomous overgrowth through pan-lineage gene expression and communication changes.

This paper presents a method to generate arterial- and venous-like endothelial cells from human iPSCs without PI3K inhibitors, enabling disease modeling of vascular disorders.

The paper introduces a non-equilibrium model explaining how signaling receptors achieve ligand specificity through multi-site phosphorylation and degradation, showing that intermediate-affinity ligands maximize network activity.

This study identifies a synergistic effect between AKT inhibitors and pitavastatin in killing triple-negative breast cancer cells by targeting cholesterol trafficking.

SIGNAL-seq measures RNA and PTMs in single cells to analyze inter- and intra-cellular signaling in the tumor microenvironment.

The paper uses single-cell analyses to show that oncogenic PIK3CAH1047R reduces IGF1 signaling specificity and enhances EGF responses, leading to increased phenotypic heterogeneity.