Laboratory for vascular biology
Biology of vascular malformations, particularly cerebral cavernous malformations (CCMs)
- Role of GCKIII proteins in cavernoma development and MAP Kinase signaling.
- Pharmacological therapies for CCMs.
The GCKIII kinases STK24 and STK25 inhibit cavernoma development
High levels of receptor tyrosine kinases in CCM3-deficient cells increase their susceptibility to tyrosine kinase inhibition
MST Kinases and Metabolism
A Functional link between ampk and orexin mediates the effect of BMP8B on energy balance.
The Cerebral Cavernous Malformation 3 gene is necessary for senescence induction
Cerebral Cavernous Malformations: from CCM genes to endothelial cell homeostasis.