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AuthorPfister, Astrid
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AbstractAutophagy represents a conserved self-digestion program, which allows regulated degradation of cellular material. Autophagy is activated by cellular stress, serum starvation and nutrient deprivation. Several autophagic pathways have been uncovered, which either non-selectively or selectively target the cellular cargo for lysosomal degradation. Autophagy engages the coordinated action of various key regulators involved in the steps of autophagosome formation, cargo targeting and lysosomal fusion. While non-selective (macro)autophagy is required for removal of bulk material or recycling of nutrients, selective autophagy mediates specific targeting of damaged organelles or protein aggregates. By proper action of the autophagic machinery, cellular homeostasis is maintained. In contrast, failure of this fundamental process is accompanied by severe pathophysiological conditions. Hallmarks of neuropathological disorders are for instance accumulated, mis-folded protein aggregates and damaged mitochondria. The nucleolus has been recognized as central hub in the cellular stress response. It represents a sub-nuclear organelle essential for ribosome biogenesis and also functions as stress sensor by mediating cell cycle arrest or apoptosis. Thus, proper nucleolar function is mandatory for cell growth and survival. Here, I highlight the emerging role of nucleolar factors in the regulation of autophagy. Moreover, I discuss the nucleolar stress response as a novel signaling pathway in the context of autophagy, health and disease.dc.description.abstract
PublisherUniversität Ulmdc.publisher
LicenseCC BY 4.0 Internationaldc.rights
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KeywordRibosome biogenesisdc.subject
KeywordrRNA processingdc.subject
KeywordNucleolar stressdc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
MeSHRNA, Ribosomaldc.subject.mesh
TitleEmerging role of the nucleolar stress response in autophagydc.title
Resource typeWissenschaftlicher Artikeldc.type
FacultyMedizinische Fakultätuulm.affiliationGeneral
InstitutionInstitut für Biochemie und Molekulare Biologieuulm.affiliationSpecific
Peer reviewjauulm.peerReview
DCMI TypeTextuulm.typeDCMI
DOI of original publication10.3389/fncel.2019.00156dc.relation1.doi
Source - Title of sourceFrontiers in Cellular Neurosciencesource.title
Source - Place of publicationFrontiers Mediasource.publisher
Source - Volume13source.volume
Source - Year2019source.year
Source - Article number156source.articleNumber
Source - eISSN1662-5102source.identifier.eissn
FundingUlm University (Baustein 3.2) [LSBN0101]uulm.funding
FundingDeutsche Krebshilfe [70112329]uulm.funding
University Bibliographyjauulm.unibibliographie

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CC BY 4.0 International
Except where otherwise noted, this item's license is described as CC BY 4.0 International