Adjunct Professor of Immunology and Infectious Diseases
08/05- HARVARD SCHOOL OF PUBLIC HEALTH, BOSTON, USA. Department of Immunology and Infectious Diseases. Postdoctoral Research Fellow. Involvement of the transcriptional factor XBP-1 in neurodegenerative disorders. Advisor: Laurie H. Glimcher, M.D.
08/04-08/05 DANA-FARBER CANCER INSTITUTE, BOSTON, USA. HOWARD HUDHES MEDICAL INSTITUTE. Department of Cancer Immunology & AIDS. Postdoctoral Research Fellow. Study of new regulatory activities of the BCL-2 protein family in the endoplasmic reticulum. Advisor: Stanley Korsmeyer, M.D.
01/02-07/04 SERONO PHARMACEUTICAL RESEARCH INSTITUTE, GENEVA, SWITZERLAND. Department of Neurobiology. PhD. In Biomedical Sciences, doctoral thesis: “The role of the Unfolded Protein Response and Endoplasmic Reticulum Stress in Prion-related disorders”. Advisor: Claudio Soto, Ph.D.
03/00-12/01 UNIVERSITY OF CHILE, SANTIAGO, CHILE. Faculty of Medicine, Institute of Biomedical Sciences. Residence of Ph.D. Study of Fas signaling in lymphoid cells involved in non-apoptotic cell death. Advisor: Andrew Quest, Ph.D.
03/95-03/00 UNIVERSITY OF CHILE, SANTIAGO, CHILE. Faculty of Sciences. Degree of Molecular Biotechnology Engineer. Degree thesis: “Cytotoxic mechanism of the bacterial forming-channel Microcin E492 in human carcinoma cells”. Advisor: Rosalba Lagos, Ph.D. and Maria R. Bono, Ph.D.
|MISSION – This laboratory focuses on understanding the molecular basis of perturbations of subcellular organelle function, their relationship to pathological conditions affecting the nervous system, and the development of prototypic therapies to prevent this damage.|
|I. ORGANELLE STRESS
Alterations in organelle function have devastating consequences for the proper function of the cell. Stress injuries initiate multiple signaling responses, either to adapt to the new conditions or to activate specific apoptosis pathways, if a critical threshold of damage has been reached. Our laboratory is committed to the study of cellular strategies involved in adaptation to chronic organelle damage, which are linked to several neurological disorders. The endoplasmic reticulum (ER) has important cellular functions, highlighting its role as a sophisticated machinery for protein folding and secretion. Alterations on ER function lead to the accumulation of unfolded proteins at its lumen, a cellular condition termed “ER stress”. ER stress engages an integrated signaling pathway known as the “Unfolded Protein Response” (UPR), which aims to restore homeostasis. Sustained ER stress ultimately promotes apoptosis, where the members of the BCL-2 family of proteins are essential in the initiation of cell death. Nevertheless, the mechanisms that control the transition from an adaptive state to cell death processes remain unknown and is a central subject of our research.
ER STRESS in PHYSIOLOGY and DISEASE
Our central research questions are:
Ph.D. in Biomedical Sciences and degree in Molecular Biotechnology Engineer