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Title:
Chaperone-mediated autophagy: roles in neuroprotection | Neuroscience Bulletin
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Chaperone-mediated autophagy (CMA), one of the main pathways of lysosomal proteolysis, is characterized by the selective targeting and direct translocation into the lysosomal lumen of substrate proteins containing a targeting motif biochemically related to the pentapeptide KFERQ. Along with the other two lysosomal pathways, macro- and micro-autophagy, CMA is essential for maintaining cellular homeostasis and survival by selectively degrading misfolded, oxidized, or damaged cytosolic proteins. CMA plays an important role in pathologies such as cancer, kidney disorders, and neurodegenerative diseases. Neurons are post-mitotic and highly susceptible to dysfunction of cellular quality-control systems. Maintaining a balance between protein synthesis and degradation is critical for neuronal functions and homeostasis. Recent studies have revealed several new mechanisms by which CMA protects neurons through regulating factors critical for their viability and homeostasis. In the current review, we summarize recent advances in the understanding of the regulation and physiology of CMA with a specifi c focus on its possible roles in neuroprotection.
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Keywords {🔍}
pubmed, article, google, scholar, cas, autophagy, central, chaperonemediated, cuervo, cell, degradation, biol, lysosomal, disease, proteins, protein, mol, dice, selective, kaushik, pathways, proteolysis, mechanisms, knecht, sci, biochem, chem, privacy, cookies, content, roles, wang, yang, cma, neuronal, nature, rev, liver, lysosomes, huntingtin, neurosci, processing, publish, search, neuroprotection, zeng, targeting, related, cellular, homeostasis,
Topics {✒️}
lys-phe-glu-arg- gln month download article/chapter bao wang & qian yang cellular quality-control systems targeting chaperone-mediated autophagy regulates chaperone-mediated autophagy chaperone-mediated autophagy markers central nervous system full article pdf chaperone-mediated autophagy privacy choices/manage cookies maintaining cellular homeostasis chiang hl intracellular protein-degradation pathways qian yang neuronal death protein quality control molecular chaperone complex chaperone carboxyl terminus article cai alpha-synuclein inclusions mutant alpha-synuclein promotes tumor growth thompson lm amino-acid deprivation ubiquitin-protein conjugates dynamic protein complexes article log neuroprotection review published related subjects survival factor mef2d european economic area modeling general proteostasis fi refi ghter confl uent conditions impaired macroautophagy rodriguez-oroz mc mutant uch-l1 uch-l1 variants retinoic acid derivatives hsp70-interacting protein peptide sequences related autophagy fights disease intracellular protein degradation conditions privacy policy tumor-suppressor form massey ac ikk phosphorylates huntingtin article cite human fibroblasts produced
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- Review: autophagy in neurodegeneration: fi refi ghter and/or incendiarist?
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headline:Chaperone-mediated autophagy: roles in neuroprotection
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datePublished:2015-07-23T00:00:00Z
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chaperone-mediated autophagy
cellular homeostasis
neuroprotection
neuronal death
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Human Physiology
Anesthesiology
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Neurology
Pain Medicine
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headline:Chaperone-mediated autophagy: roles in neuroprotection
description:Chaperone-mediated autophagy (CMA), one of the main pathways of lysosomal proteolysis, is characterized by the selective targeting and direct translocation into the lysosomal lumen of substrate proteins containing a targeting motif biochemically related to the pentapeptide KFERQ. Along with the other two lysosomal pathways, macro- and micro-autophagy, CMA is essential for maintaining cellular homeostasis and survival by selectively degrading misfolded, oxidized, or damaged cytosolic proteins. CMA plays an important role in pathologies such as cancer, kidney disorders, and neurodegenerative diseases. Neurons are post-mitotic and highly susceptible to dysfunction of cellular quality-control systems. Maintaining a balance between protein synthesis and degradation is critical for neuronal functions and homeostasis. Recent studies have revealed several new mechanisms by which CMA protects neurons through regulating factors critical for their viability and homeostasis. In the current review, we summarize recent advances in the understanding of the regulation and physiology of CMA with a specifi c focus on its possible roles in neuroprotection.
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