Juan Zalvide Group



Juan Zalvide obtained his medical degree in 1989, in the University of Santiago de Compostela. Four years later, in 1993, he read his Thesis and obtained his PhD degree in the same University. Thereafter, he was a postdoctoral fellow at the Dana-Farber Cancer Institute, Harvard University, in Boston, USA. He joined back the Department of Physiology in the University of Santiago de Compostela in 1996. He is Associate Professor since 2002.Juan Zalvide

Research group

Research lines


The group is interested in cell biology and its applications to biomedicine. After studying cell cycle regulation in cancer cells, we are now focusing in the biology of CCM proteins, which mutation predisposes to vascular malformations. We have shown that one of the CCM proteins, CCM3, is important both for Golgi morphogenesis and for protection against stress. We are now investigating how these actions relate to cell morphology and endothelial cell biology. This will lead to new strategies for vascular malformation prevention and handling .
Follow this link to learn on CCM3 biology.


Ongoing projects

  • CCM3/PDCD10 and Mst kinases. Role in the pathogenesis of Cerebral Cavernous Malformations. Instituto de Salud Carlos III. (PI: J. Zalvide).
  • Cerebral Cavernous Malformations. From pathobiology to therapeutic strategies. ERA-NET neuron. (PI: J. Zalvide).

Articles last five years

  • C. Pombo, T. Force, J.Kyriakis, E. Nogueira, M. Fidalgo, J.Zalvide (2007) The GCK II and III subfamilies of the STE20 group kinases. Frontiers in Bioscience 12: 850-9. Link.
  • A. Vidal, C. Carneiro, J. Zalvide (2007) Of mice without pockets: mouse models to study the function of the Rb family. Frontiers in Bioscience 12: 4483-96. Link.
  • A. Solloso, L. Barreiro, R. Seoane, E. Nogueira, C. Cañibano, C.V. Álvarez, J. Zalvide, C. Diéguez, C.Pombo (2008) GHRH proliferative action on somatotrophs is cell-type specific and dependent on Pit-1/GHF-1 expression. J. Cell Physiol. 215(1): 140-50. Link.
  • E. Nogueira, M. Fidalgo, A. Molnar, J. Kyriakis, T. Force, J. Zalvide, C. Pombo (2008). SOK1 translocates from the Golgi to the nucleus upon oxidative stress and induces apoptotic cell death. J. Biol. Chem. 283(23):16248-58. Link.
  • M. Santamariña, G. Hernández, J. Zalvide (2008) Cdk redundancy guarantees cell cycle progression in Rb-negative tumor cells independently of their p16 status. Cell Cycle. 7(13):1962-72. Link.
  • M. Fidalgo, M. Fraile, A. Pires, T. Force, C.M. Pombo, J. Zalvide (2010) CCM3/PDCD10 stabilizes GCKIII proteins to promote Golgi assembly and cell orientation. J. Cell Sci. 123: 1274-84. Link.
  • G. Hernandez, H. Lal, M.l Fidalgo, A. Guerrero, J. Zalvide, T. Force, C. M. Pombo (2011) A novel cardioprotective p38-MAPK/mTOR pathway.  Experimental Cell Research, 317(20):2938-49. Link.
  • M. Fidalgo, A. Guerrero, M. Fraile, C. Iglesias, C.M. Pombo. J. Zalvide (2012) The adaptor protein cerebral cavernous malformation 3 (CCM3) mediates phosphorylation of the cytoskeletal proteins Ezrin/Radixin/Moesin by Mammalian Ste20-4 to protect cells from oxidative stress. J. Biol. Chem. 287: 11556-11565. Link.
  • A. Fischer, J. Zalvide, E. Faurobert, C. Albiges-Rizo, E. Tournier-Lasserve. Cerebral Cavernous Malformations: from CCM genes to endothelial cell homeostasis. Trends in Molecular Medicine. 2013. In press.
  • J. Zalvide, M. Fidalgo, M. Fraile, A. Guerrero, C. Iglesias, E. Floridia, C. M. Pombo. The CCM3-GCKIII partnership (2013). Histology and Histopathology. In press. Link.