Heat shock proteins: Cellular and molecular mechanisms in the central nervous system |
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Authors: | R. Anne Stetler Yu Gan Wenting Zhang Anthony K. Liou Yanqin Gao Guodong Cao Jun Chen |
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Affiliation: | 1. Geriatric Research, Educational and Clinical Center, Veterans Affairs Pittsburgh Health Care System, Pittsburgh, PA 15261, United States;2. State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China;3. Center of Cerebrovascular Disease Research, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, United States |
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Abstract: | Emerging evidence indicates that heat shock proteins (HSPs) are critical regulators in normal neural physiological function as well as in cell stress responses. The functions of HSPs represent an enormous and diverse range of cellular activities, far beyond the originally identified roles in protein folding and chaperoning. HSPs are now understood to be involved in processes such as synaptic transmission, autophagy, ER stress response, protein kinase and cell death signaling. In addition, manipulation of HSPs has robust effects on the fate of cells in neurological injury and disease states. The ongoing exploration of multiple HSP superfamilies has underscored the pluripotent nature of HSPs in the cellular context, and has demanded the recent revamping of the nomenclature referring to these families to reflect a re-organization based on structure and function. In keeping with this re-organization, we first discuss the HSP superfamilies in terms of protein structure, regulation, expression and distribution in the brain. We then explore major cellular functions of HSPs that are relevant to neural physiological states, and from there we discuss known and proposed HSP impacts on major neurological disease states. This review article presents a three-part discussion on the array of HSP families relevant to neuronal tissue, their cellular functions, and the exploration of therapeutic targets of these proteins in the context of neurological diseases. |
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Keywords: | AChR, acetylcholine receptor AD, Alzheimer's disease AIF, apoptosis-inducing factor APP, amyloid precursor protein ARE, AU-rich elements CHIP, C-terminal HSP-interacting protein CMA, chaperone-mediated autophagy CMT, Charcot&ndash Marie&ndash Tooth dHMN, distal hereditary motor neuropathy ERAD, endoplasmic reticulum-associated degradation GA, geldanamycin G/F, glycine/phenylalanine HD, Huntington's disease Hip, heat shock factor interacting protein Hop, heat shock factor organizing protein HSE, heat shock element HSF, heat shock factor HSP, heat shock protein HSR, heat shock response KA, kainic acid LAMP2A, lysosome-associated membrane protein 2 MCAO, middle cerebral artery occlusion mtUPR, mitochondrial unfolded protein response NEF, nucleotide exchange factor NMJ, neuromuscular junction PD, Parkinson's disease PERK, PKR-like ER kinase polyQ, polyglutamine PP5, protein phosphatase 5 PPD, polypeptide domain PS1, presenilin-1 ROS, reactive oxygen species SCA, spinocerebellar ataxia SNARE, soluble NSF attachment protein receptors TIM, translocase of inner membrane TOM, translocase of outer membrane TPR, tetratricopeptide repeats TSE, transmissible spongiform encephalopathies UPR, unfolded protein response |
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