Juan Carlos Zabala
Departamento de Biología Molecular
Unidad Asociada al CIB-CSIC
Facultad de Medicina
Santander-39011, Spain
Phone: (34) 942 - 2 20 - 1949
Fax: (34) 942 - 201 - 945


Degree in Pharmacy University of Santiago de Compostela. Spain, 1978. Ph.D. awarded July, 1982. University of Santiago de Compostela. Spain. He is Associate Professor at the Department of Molecular Biology. Faculty of Medicine. University of Cantabria. Spain. From 1977 to 1978 he received an student fellowship "Beca del Instituto Nacional de Ayuda y Promoción del Estudiante", from the Spanish Ministry of Education (1977-1978). Recipient of a Doctoral Fellowship "Beca de Formación del Personal Investigador" from the Spanish Ministry of Education (1979-1981). Recipient of a Postdoctoral Fellowship from the NATO (1987-1988). Cowan’s lab in NYU Medical School. USA Recipient of a Fogarty International Research fellowship from the National Institutes of Health (1988-1989). Cowan’s lab in NYU Medical School. USA. Recipient of a fellowship from the Spanish Ministry of Education (1999-2000). Visiting scholar at Stearns’ lab in the Dept of Biological Sciences, Stanford University USA.

Scientific interests

We hypothesize that the tubulin folding pathway, controlling the synthesis and flux of mature tubulin heterodimers, plays a central role in regulating the assembly, remodelling and dynamics of microtubule structures. Our interest is to achieve a better understanding of the structure and function of the mammalian tubulin folding cofactors (TBCs). It must be emphasized that several of the cofactors have been linked to human diseases. Understanding the in vivo function of these proteins will shed light on the Kenny-Caffey/Sanjad-Sakati syndrome (HRD), an important human disorder associated with TBCE. We have also shown that TBCB localizes at the extremes of growing neurites during neurogenesis where it plays a role in growth cone microtubule dynamics and plasticity. Gene silencing, by means of small interfering RNA segments, revealed that TBCB knockdown enhances axonal growth. In contrast, TBCB excess, a feature of Giant Axonal Neuropathy, leads to microtubule depolymerization, growth cone retraction and axonal damage followed by neuronal degeneration. Our group in Santander, in collaboration with two different Departments of the Hospital Universitario Marqués de Valdecilla, is also trying to characterize the pathophysiology of HRD, and other diseases which might be related to these cofactors.

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