DOI . ORG {
}
We began analyzing https://link.springer.com/article/10.1007/s00018-010-0565-6, but it redirected us to https://link.springer.com/article/10.1007/s00018-010-0565-6. The analysis below is for the second page.
Title[redir]:
Chaperone-mediated autophagy: machinery, regulation and biological consequences | Cellular and Molecular Life Sciences
Description:
Degradation of dysfunctional intracellular components in the lysosome system can occur through three different pathways, i.e., macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). In this review, we focus on CMA, a type of autophagy distinct from the other two autophagic pathways owing to its selectivity, saturability and competitivity by which a subset of long-lived cytosolic soluble proteins are directly delivered into the lysosomal lumen via specific receptors. CMA participates in quality control to maintain normal cell functions by clearing “old” proteins and provides energy to cells under nutritional stress. Deregulation of CMA has recently been shown to underlie some diseases, especially neurodegenerative disorders for which the decline with age in the activity of CMA may become a major aggravating factor. Therefore, targeting aberrant alteration in CMA under pathological conditions could serve as a potential therapeutic strategy for treating related diseases.
Title[redir]:
Chaperone-mediated autophagy: machinery, regulation and biological consequences | Cellular and Molecular Life Sciences
Description:
Degradation of dysfunctional intracellular components in the lysosome system can occur through three different pathways, i.e., macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). In this review, we focus on CMA, a type of autophagy distinct from the other two autophagic pathways owing to its selectivity, saturability and competitivity by which a subset of long-lived cytosolic soluble proteins are directly delivered into the lysosomal lumen via specific receptors. CMA participates in quality control to maintain normal cell functions by clearing “old” proteins and provides energy to cells under nutritional stress. Deregulation of CMA has recently been shown to underlie some diseases, especially neurodegenerative disorders for which the decline with age in the activity of CMA may become a major aggravating factor. Therefore, targeting aberrant alteration in CMA under pathological conditions could serve as a potential therapeutic strategy for treating related diseases.
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Keywords {🔍}
google, scholar, pubmed, cas, autophagy, chaperonemediated, cuervo, biol, cell, dice, degradation, chem, lysosomal, mol, proteins, selective, protein, article, kaushik, mao, molecular, pathways, cma, disease, cellular, regulation, lysosome, factor, wang, lysosomes, mechanisms, ubiquitin, biochem, nat, sci, membrane, massey, privacy, cookies, content, macroautophagy, functions, cells, role, saftig, nature, knecht, alphasynuclein, kiffin, function,
Topics {✒️}
lamp-1/lamp-2 double-deficient fibroblasts month download article/chapter qian yang & zixu mao abnormal chaperone-mediated autophagy harnessing chaperone-mediated autophagy chaperone-mediated autophagy depends regulates chaperone-mediated autophagy stress-regulated cochaperone aha1 chaperone-assisted selective autophagy lamp-2-deficient mice myocyte-enhancer factor 2 potential therapeutic strategy privacy choices/manage cookies mutant alpha-synuclein camp-protein kinase transcription factor mef2 chaperone carboxyl terminus full article pdf ubiquitin ligase complexes autophagy-lysosomal degradation pathway manning-bog ab chaperone-mediated autophagy chaperone mediated autophagy neurotoxicity-induced apoptosis chemically induced nephropathy senescent human fibroblasts mutant uch-l1 molecular chaperone complex ubiquitin-mediated recognition chaperone-assisted degradation major aggravating factor nucleotide exchange factor cdk5-mediated inhibition related subjects eskelinen el autophagy-lysosome systems european economic area glyceraldehyde-3-phosphate dehydrogenase auxilindynamin interactions link uncouples nucleotide hydrolysis peptide sequences related di monte da ikk phosphorylates huntingtin acute diabetes mellitus fox foundation grant emory university school protein half-lives dynamic protein complexes mutant huntingtin protein normal proteolytic function
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headline:Chaperone-mediated autophagy: machinery, regulation and biological consequences
description:Degradation of dysfunctional intracellular components in the lysosome system can occur through three different pathways, i.e., macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). In this review, we focus on CMA, a type of autophagy distinct from the other two autophagic pathways owing to its selectivity, saturability and competitivity by which a subset of long-lived cytosolic soluble proteins are directly delivered into the lysosomal lumen via specific receptors. CMA participates in quality control to maintain normal cell functions by clearing “old” proteins and provides energy to cells under nutritional stress. Deregulation of CMA has recently been shown to underlie some diseases, especially neurodegenerative disorders for which the decline with age in the activity of CMA may become a major aggravating factor. Therefore, targeting aberrant alteration in CMA under pathological conditions could serve as a potential therapeutic strategy for treating related diseases.
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description:Degradation of dysfunctional intracellular components in the lysosome system can occur through three different pathways, i.e., macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). In this review, we focus on CMA, a type of autophagy distinct from the other two autophagic pathways owing to its selectivity, saturability and competitivity by which a subset of long-lived cytosolic soluble proteins are directly delivered into the lysosomal lumen via specific receptors. CMA participates in quality control to maintain normal cell functions by clearing “old” proteins and provides energy to cells under nutritional stress. Deregulation of CMA has recently been shown to underlie some diseases, especially neurodegenerative disorders for which the decline with age in the activity of CMA may become a major aggravating factor. Therefore, targeting aberrant alteration in CMA under pathological conditions could serve as a potential therapeutic strategy for treating related diseases.
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