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AuthorKreiner, Grzegorzdc.contributor.author
AuthorSönmez, Aynurdc.contributor.author
AuthorLiß, Birgitdc.contributor.author
AuthorParlato, Rosannadc.contributor.author
Date of accession2021-10-20T13:27:29Zdc.date.accessioned
Available in OPARU since2021-10-20T13:27:29Zdc.date.available
Date of first publication2019-04-26dc.date.issued
AbstractUnderstanding underlying mechanisms of neurodegenerative diseases is fundamental to develop effective therapeutic intervention. Yet they remain largely elusive, but metabolic, and transcriptional dysregulation are common events. Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NADC)-dependent lysine deacetylase, regulating transcription, and critical for the cellular adaptations to metabolic stress. SIRT1 regulates the transcription of ribosomal RNA (rRNA), connecting the energetic state with cell growth and function. The activity of the transcription initiation factor-IA (TIF-IA) is important for the transcriptional regulation of ribosomal DNA (rDNA) genes in the nucleolus, and is also sensitive to changes in the cellular energetic state. Moreover, TIF-IA is responsive to nutrient-deprivation, neurotrophic stimulation, and oxidative stress. Hence, both SIRT1 and TIF-IA connect changes in cellular stress with transcriptional regulation and metabolic adaptation. Moreover, they finely tune the activity of the transcription factor p53, maintain mitochondrial function, and oxidative stress responses. Here we reviewed and discussed evidence that SIRT1 and TIF-IA are regulated by shared pathways and their activities preserve neuronal homeostasis in response to metabolic stressors. We provide evidence that loss of rDNA transcription due to altered TIF-IA function alters SIRT1 expression and propose a model of interdependent feedback mechanisms. An imbalance of this signaling might be a critical common event in neurodegenerative diseases. In conclusion, we provide a novel perspective for the prediction of the therapeutic benefits of the modulation of SIRT1- and nucleolar-dependent pathways in metabolic and neurodegenerative diseases.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseCC BY 4.0 Internationaldc.rights
Link to license texthttp://creativecommons.org/licenses/by/4.0/dc.rights.uri
Keywordnucleolusdc.subject
KeywordrRNAdc.subject
Keywordneuronal homeostasisdc.subject
Keywordneurodegenerationdc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
LCSHNervous system; Degenerationdc.subject.lcsh
MeSHNeurodegenerative diseasesdc.subject.mesh
MeSHSirtuinsdc.subject.mesh
MeSHOxidative stressdc.subject.mesh
MeSHRNA, Ribosomaldc.subject.mesh
TitleIntegration of the deacetylase SIRT1 in the response to nucleolar stress:metabolic implications for neurodegenerative diseasesdc.title
Resource typeWissenschaftlicher Artikeldc.type
SWORD Date2020-01-28T13:25:15Zdc.date.updated
VersionpublishedVersiondc.description.version
DOIhttp://dx.doi.org/10.18725/OPARU-39182dc.identifier.doi
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-oparu-39258-6dc.identifier.urn
GNDNervendegenerationdc.subject.gnd
GNDSirtuinedc.subject.gnd
GNDOxidativer Stressdc.subject.gnd
GNDRibosomale RNSdc.subject.gnd
GNDProtein p53dc.subject.gnd
FacultyMedizinische Fakultätuulm.affiliationGeneral
InstitutionInstitut für Allgemeine Physiologieuulm.affiliationSpecific
Peer reviewjauulm.peerReview
DCMI TypeTextuulm.typeDCMI
CategoryPublikationenuulm.category
In cooperation withPolish Academy of Sciencesuulm.cooperation
In cooperation withUniversity of Oxforduulm.cooperation
In cooperation withUniversität Heidelberguulm.cooperation
DOI of original publication10.3389/fnmol.2019.00106dc.relation1.doi
Source - Title of sourceFrontiers in Molecular Neurosciencesource.title
Source - Place of publicationFrontiers Mediasource.publisher
Source - Volume12source.volume
Source - Year2019source.year
Source - Article number106source.articleNumber
Source - eISSN1662-5099source.identifier.eissn
FundingDFG [PA 1529/2-1]uulm.funding
FundingDFG [LI-1745/1]uulm.funding
FundingGRK 1789: Zelluläre und molekulare Mechanismen der Alterung / DFG [194266605]uulm.funding
FundingSFB F-4410 / FWFuulm.funding
FundingAlfried Krupp Foundationuulm.funding
FundingNCN OPUS 13 / National Science Center [2017/25/B/NZ7/02406]uulm.funding
Bibliographyuulmuulm.bibliographie


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