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dc.contributor.authorPage, MM
dc.contributor.authorSchuster, EF
dc.contributor.authorMudaliar, M
dc.contributor.authorHerzyk, P
dc.contributor.authorWithers, DJ
dc.contributor.authorSelman, C
dc.date.accessioned2019-03-04T14:39:15Z
dc.date.issued2018-05
dc.identifier.citationAging, 2018, 10 (5), pp. 1027 - 1052
dc.identifier.issn1945-4589
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3114
dc.identifier.eissn1945-4589
dc.identifier.doi10.18632/aging.101446
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 (WT AL and KO AL ) or fed a 30% DR diet (WT DR or KO DR ). Using an RNAseq approach we noted a high correlation coefficient of differentially expressed genes existed within the same tissue across WT DR and KO AL 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 KO AL and KO DR , 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.
dc.formatPrint
dc.format.extent1027 - 1052
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectAnimals
dc.subjectMice, Knockout
dc.subjectMice
dc.subjectCaloric Restriction
dc.subjectTranscription, Genetic
dc.subjectLongevity
dc.subjectInsulin Receptor Substrate Proteins
dc.titleCommon and unique transcriptional responses to dietary restriction and loss of insulin receptor substrate 1 (IRS1) in mice.
dc.typeJournal Article
dcterms.dateAccepted2018-05-08
rioxxterms.versionofrecord10.18632/aging.101446
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2018-05
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfAging
pubs.declined2019-03-01T15:50:03.571+0000
pubs.issue5
pubs.notesNo embargo
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/Endocrine Therapy Resistance
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/Endocrine Therapy Resistance
pubs.publication-statusPublished
pubs.volume10
pubs.embargo.termsNo embargo
icr.researchteamEndocrine Therapy Resistanceen_US
dc.contributor.icrauthorSchuster, Eugeneen


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