Research Topics
Genomes and Genes | Claudio A HetzSummaryAffiliation: Harvard University Country: USA Publications
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Publications
Stressing out the ER: a role of the unfolded protein response in prion-related disordersClaudio A Hetz
Harvard School of Public Health, Department of Immunology and Infectious Diseases, Boston, MA 02115, USA
Curr Mol Med 6:37-43. 2006..These findings have applications for developing novel strategies for treatment and early diagnosis of transmissible spongiform encephalopathies and other neurodegenerative diseases...
Autophagy impairment: a crossroad between neurodegeneration and tauopathiesMelissa Nassif
Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile
BMC Biol 10:78. 2012..We discuss the implications of this study for understanding the factors driving neurofibrillary tangle formation in Alzheimer's disease and tauopathies...
The unfolded protein response: controlling cell fate decisions under ER stress and beyondClaudio Hetz
Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, P O BOX 70086, Chile
Nat Rev Mol Cell Biol 13:89-102. 2012..In addition, novel physiological outcomes of the UPR that are not directly related to protein-folding stress, such as innate immunity, metabolism and cell differentiation, have been revealed...
Proapoptotic BAX and BAK modulate the unfolded protein response by a direct interaction with IRE1alphaClaudio Hetz
Howard Hughes Medical Institute, Dana Farber Cancer Institute, and Harvard Medical School, Boston, MA 02115, USA
Science 312:572-6. 2006..Thus, BAX and BAK function at the ER membrane to activate IRE1alpha signaling and to provide a physical link between members of the core apoptotic pathway and the UPR...
Unfolded protein response transcription factor XBP-1 does not influence prion replication or pathogenesisClaudio Hetz
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 105:757-62. 2008....
Cyclophilin D is a component of mitochondrial permeability transition and mediates neuronal cell death after focal cerebral ischemiaAnna C Schinzel
Howard Hughes Medical Institute and Dana Farber Cancer Institute, Harvard Medical School, 44 Binney Street, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 102:12005-10. 2005....
The daily job of night killers: alternative roles of the BCL-2 family in organelle physiologyClaudio Hetz
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
Trends Cell Biol 18:38-44. 2008..Here, we describe the emerging concept that BCL-2-related proteins have alternative functions beyond apoptosis to control the essential functions of the cell...
ER stress signaling and the BCL-2 family of proteins: from adaptation to irreversible cellular damageClaudio A Hetz
Department of Cellular and Molecular Biology, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile and the FONDAP Center for Molecular Studies of the Cell CEMC, Santiago, Chile
Antioxid Redox Signal 9:2345-55. 2007..Thus, BCL-2-related proteins are not only the "death gateway" keepers, but they also have alternative functions in essential cellular processes...
Prion pathogenesis is independent of caspase-12Andrew D Steele
Whitehead Institute for Biomedical Research, Howard Hughes Medical Institute, Massachusets Institute of Technology, Cambridge Massachusetts 02142, USA
Prion 1:243-7. 2007....
Diminishing apoptosis by deletion of Bax or overexpression of Bcl-2 does not protect against infectious prion toxicity in vivoAndrew D Steele
Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA
J Neurosci 27:13022-7. 2007..These results suggest that Bax and Bcl-2 mediated apoptotic pathways are not the major contributing factor to the clinical or pathological features of infectious prion disease...
Emerging roles of the unfolded protein response signaling in physiology and diseaseClaudio A Hetz
Curr Mol Med 6:1. 2006
