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Retinoic Acid Signalling in the Pineal Gland Is Conserved across Mammalian Species and Its Transcriptional Activity Is Inhibited by Melatonin

dc.contributor.authorAshton, Anna
dc.contributor.authorClark, Jason
dc.contributor.authorFedo, Julia
dc.contributor.authorSementilli, Angelo
dc.contributor.authorFragoso, Yara D
dc.contributor.authorMcCaffery, Peter
dc.date.accessioned2024-02-07T08:18:46Z
dc.date.available2024-02-07T08:18:46Z
dc.date.issued2023-01-11
dc.identifier227046831
dc.identifier7e1f007e-bc23-4837-b1d3-260bc41534ce
dc.identifier36672220
dc.identifier85146738316
dc.identifier.citationAshton , A , Clark , J , Fedo , J , Sementilli , A , Fragoso , Y D & McCaffery , P 2023 , ' Retinoic Acid Signalling in the Pineal Gland Is Conserved across Mammalian Species and Its Transcriptional Activity Is Inhibited by Melatonin ' , Cells , vol. 12 , no. 2 , 286 . https://doi.org/10.3390/cells12020286en
dc.identifier.issn2073-4409
dc.identifier.otherPubMedCentral: PMC9856906
dc.identifier.otherORCID: /0000-0002-5956-3997/work/129408653
dc.identifier.urihttp://aura-test.abdn.ac.uk/handle/2164/20097
dc.descriptionThis article belongs to the Collection Functions of Nuclear Receptors Acknowledgments We thank David Hazlerigg for providing the MSM mice. qPCR was performed with the help of the Institute of Medical Sciences qPCR Core Facility at the University of Aberdeen.en
dc.format.extent15
dc.format.extent1927917
dc.language.isoeng
dc.relation.ispartofCellsen
dc.subjectRatsen
dc.subjectMiceen
dc.subjectHumansen
dc.subjectAnimalsen
dc.subjectPineal Gland/metabolismen
dc.subjectMelatonin/pharmacologyen
dc.subjectTretinoin/pharmacologyen
dc.subjectSignal Transductionen
dc.subjectMammals/metabolismen
dc.subjectQ Scienceen
dc.subject.lccQen
dc.titleRetinoic Acid Signalling in the Pineal Gland Is Conserved across Mammalian Species and Its Transcriptional Activity Is Inhibited by Melatoninen
dc.typeJournal articleen
dc.contributor.institutionUniversity of Aberdeen.Medicine, Medical Sciences & Nutritionen
dc.contributor.institutionUniversity of Aberdeen.Institute of Medical Sciencesen
dc.contributor.institutionUniversity of Aberdeen.Medical Sciencesen
dc.contributor.institutionUniversity of Aberdeen.Neuroscienceen
dc.description.statusPeer revieweden
dc.identifier.doihttps://doi.org/10.3390/cells12020286
dc.identifier.vol12en
dc.identifier.iss2en


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