At the end of the autophagic road: an emerging understanding of lysosomal functions in autophagy.
Identifieur interne : 000F23 ( Main/Exploration ); précédent : 000F22; suivant : 000F24At the end of the autophagic road: an emerging understanding of lysosomal functions in autophagy.
Auteurs : Han-Ming Shen [Singapour] ; Noboru Mizushima [Japon]Source :
- Trends in biochemical sciences [ 0968-0004 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Arabidopsis (génétique), Arabidopsis (métabolisme), Autophagie (génétique), Complexe-1 cible mécanistique de la rapamycine (MeSH), Complexes multiprotéiques (génétique), Complexes multiprotéiques (métabolisme), Extracellular Signal-Regulated MAP Kinases (génétique), Extracellular Signal-Regulated MAP Kinases (métabolisme), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (génétique), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (métabolisme), Humains (MeSH), Lysosomes (anatomopathologie), Lysosomes (métabolisme), Maladies neurodégénératives (anatomopathologie), Maladies neurodégénératives (génétique), Maladies neurodégénératives (métabolisme), Phagosomes (anatomopathologie), Phagosomes (métabolisme), Protéines SNARE (génétique), Protéines SNARE (métabolisme), Régulation de l'expression des gènes (MeSH), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH).
- MESH :
- anatomopathologie : Lysosomes, Maladies neurodégénératives, Phagosomes.
- génétique : Arabidopsis, Autophagie, Complexes multiprotéiques, Extracellular Signal-Regulated MAP Kinases, Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines, Maladies neurodégénératives, Protéines SNARE, Saccharomyces cerevisiae, Sérine-thréonine kinases TOR.
- métabolisme : Arabidopsis, Complexes multiprotéiques, Extracellular Signal-Regulated MAP Kinases, Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines, Lysosomes, Maladies neurodégénératives, Phagosomes, Protéines SNARE, Saccharomyces cerevisiae, Sérine-thréonine kinases TOR.
- Animaux, Complexe-1 cible mécanistique de la rapamycine, Humains, Régulation de l'expression des gènes, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Arabidopsis (genetics), Arabidopsis (metabolism), Autophagy (genetics), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (genetics), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism), Extracellular Signal-Regulated MAP Kinases (genetics), Extracellular Signal-Regulated MAP Kinases (metabolism), Gene Expression Regulation (MeSH), Humans (MeSH), Lysosomes (metabolism), Lysosomes (pathology), Mechanistic Target of Rapamycin Complex 1 (MeSH), Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Neurodegenerative Diseases (genetics), Neurodegenerative Diseases (metabolism), Neurodegenerative Diseases (pathology), Phagosomes (metabolism), Phagosomes (pathology), SNARE Proteins (genetics), SNARE Proteins (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , genetics : Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Extracellular Signal-Regulated MAP Kinases, Multiprotein Complexes, SNARE Proteins, TOR Serine-Threonine Kinases.
- genetics : Arabidopsis, Autophagy, Neurodegenerative Diseases, Saccharomyces cerevisiae.
- metabolism : Arabidopsis, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Extracellular Signal-Regulated MAP Kinases, Lysosomes, Multiprotein Complexes, Neurodegenerative Diseases, Phagosomes, SNARE Proteins, Saccharomyces cerevisiae, TOR Serine-Threonine Kinases.
- pathology : Lysosomes, Neurodegenerative Diseases, Phagosomes.
- Animals, Gene Expression Regulation, Humans, Mechanistic Target of Rapamycin Complex 1, Signal Transduction.
Abstract
In the past decade, autophagy studies have largely focused on the early stage of autophagy: the molecular mechanisms leading to autophagosome formation. Recently, however, we have observed significant progress in understanding the role of lysosomes, the specific cellular organelle that degrades cellular components delivered via autophagy. The discoveries include connections between autophagy and lysosomal biogenesis, activation, reformation, and turnover, as well as the identification of an autophagosomal SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) protein in control of autophagosome-lysosome fusion. We illustrate these findings in the context of the underlying molecular mechanisms and the relevance to human health and disease.
DOI: 10.1016/j.tibs.2013.12.001
PubMed: 24369758
Affiliations:
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Recently, however, we have observed significant progress in understanding the role of lysosomes, the specific cellular organelle that degrades cellular components delivered via autophagy. The discoveries include connections between autophagy and lysosomal biogenesis, activation, reformation, and turnover, as well as the identification of an autophagosomal SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) protein in control of autophagosome-lysosome fusion. We illustrate these findings in the context of the underlying molecular mechanisms and the relevance to human health and disease. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24369758</PMID><DateCompleted><Year>2014</Year><Month>06</Month><Day>25</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0968-0004</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Trends in biochemical sciences</Title><ISOAbbreviation>Trends Biochem Sci</ISOAbbreviation></Journal><ArticleTitle>At the end of the autophagic road: an emerging understanding of lysosomal functions in autophagy.</ArticleTitle><Pagination><MedlinePgn>61-71</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.tibs.2013.12.001</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0968-0004(13)00200-4</ELocationID><Abstract><AbstractText>In the past decade, autophagy studies have largely focused on the early stage of autophagy: the molecular mechanisms leading to autophagosome formation. Recently, however, we have observed significant progress in understanding the role of lysosomes, the specific cellular organelle that degrades cellular components delivered via autophagy. The discoveries include connections between autophagy and lysosomal biogenesis, activation, reformation, and turnover, as well as the identification of an autophagosomal SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) protein in control of autophagosome-lysosome fusion. We illustrate these findings in the context of the underlying molecular mechanisms and the relevance to human health and disease. </AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Han-Ming</ForeName><Initials>HM</Initials><AffiliationInfo><Affiliation>Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore. 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