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dc.contributor.authorPage, MMen_US
dc.contributor.authorSchuster, EFen_US
dc.contributor.authorMudaliar, Men_US
dc.contributor.authorHerzyk, Pen_US
dc.contributor.authorWithers, DJen_US
dc.contributor.authorSelman, Cen_US
dc.coverage.spatialUnited Statesen_US
dc.date.accessioned2019-03-04T14:39:15Z
dc.date.issued2018-05-20en_US
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/29779018en_US
dc.identifier101446en_US
dc.identifier.citationAging (Albany NY), 2018, 10 (5), pp. 1027 - 1052en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3114
dc.identifier.eissn1945-4589en_US
dc.identifier.doi10.18632/aging.101446en_US
dc.description.abstractDietary restriction (DR) is the most widely studied non-genetic intervention capable of extending lifespan across multiple taxa. Modulation of genes, primarily within the insulin/insulin-like growth factor signalling (IIS) and the mechanistic target of rapamycin (mTOR) signalling pathways also act to extend lifespan in model organisms. For example, mice lacking insulin receptor substrate-1 (IRS1) are long-lived and protected against several age-associated pathologies. However, it remains unclear how these particular interventions act mechanistically to produce their beneficial effects. Here, we investigated transcriptional responses in wild-type and IRS1 null mice fed an ad libitum diet (WTAL and KOAL) or fed a 30% DR diet (WTDR or KODR). Using an RNAseq approach we noted a high correlation coefficient of differentially expressed genes existed within the same tissue across WTDR and KOAL mice and many metabolic features were shared between these mice. Overall, we report that significant overlap exists in the tissue-specific transcriptional response between long-lived DR mice and IRS1 null mice. However, there was evidence of disconnect between transcriptional signatures and certain phenotypic measures between KOAL and KODR, in that additive effects on body mass were observed but at the transcriptional level DR induced a unique set of genes in these already long-lived mice.en_US
dc.format.extent1027 - 1052en_US
dc.languageengen_US
dc.language.isoengen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectdietary restrictionen_US
dc.subjectinsulin receptor substrate 1en_US
dc.subjectinsulin/IGF-1 signallingen_US
dc.subjectlifespanen_US
dc.subjecttranscriptomicsen_US
dc.subjectAnimalsen_US
dc.subjectCaloric Restrictionen_US
dc.subjectInsulin Receptor Substrate Proteinsen_US
dc.subjectLongevityen_US
dc.subjectMiceen_US
dc.subjectMice, Knockouten_US
dc.subjectTranscription, Geneticen_US
dc.titleCommon and unique transcriptional responses to dietary restriction and loss of insulin receptor substrate 1 (IRS1) in mice.en_US
dc.typeJournal Article
dcterms.dateAccepted2018-05-08en_US
rioxxterms.versionofrecord10.18632/aging.101446en_US
rioxxterms.licenseref.startdate2018-05-20en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfAging (Albany NY)en_US
pubs.issue5en_US
pubs.notesNo embargoen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Endocrinology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Endocrinology
pubs.publication-statusPublisheden_US
pubs.volume10en_US
pubs.embargo.termsNo embargoen_US
icr.researchteamEndocrinologyen_US
dc.contributor.icrauthorSchuster, Eugeneen_US


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Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by/4.0/