Crosstalk between the UPR and autophagy pathway contributes to handling cellular stress in neurodegenerative disease英文电子书.pdf

Crosstalk between the UPR and autophagy pathway contributes to handling cellular stress in neurodegenerative disease英文电子书.pdf

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Autophagy 8:6, 970–972; June 2012; G 2012 Landes Bioscience Crosstalk between the UPR and autophagy pathway contributes to handling cellular stress in neurodegenerative disease Rene L. Vidal1,2 and Claudio Hetz1,2,3,4,* 1Biomedical Neuroscience Institute; Faculty of Medicine; University of Chile; Santiago, Chile; 2Center for Molecular Studies of the Cell; Institute of Biomedical Sciences; University of Chile; Santiago, Chile; 3Department of Immunology and Infectious Diseases; Harvard School of Public Health; Boston, MA USA; 4Neurounion Biomedical Foundation; Santiago, Chile Huntington disease (HD) is caused is becoming a relevant target for disease by an extended polyglutamine intervention in most neurodegenerative [poly(Q)] stretch in the Huntingtin diseases. Protein homeostasis is currently (HTT) protein, and is associated with viewed as a dynamic network of signaling the accumulation of intracellular protein events that constantly adjust perturbation aggregates, onset of progressive chorea, in every step of protein folding/synthesis © 2012 Landes Bioscience. psychiatric symptoms and dementia. and degradation of proteins. This homeo- Although the mechanism underlying the static balance has been evidenced by pathological effects of mutant HTT many studies in the HD field where

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