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dc.contributor.authorÖncül, Merve
dc.contributor.authorDilsiz, Pelin
dc.contributor.authorAteş Öz, Edanur
dc.contributor.authorAteş, Tayfun
dc.contributor.authorAklan, İltan
dc.contributor.authorÇelik, Eşref
dc.contributor.authorSayar Atasoy, Nilüfer
dc.contributor.authorAtasoy, Deniz
dc.date.accessioned10.07.201910:49:13
dc.date.accessioned2019-07-10T19:50:13Z
dc.date.available10.07.201910:49:13
dc.date.available2019-07-10T19:50:13Z
dc.date.issued2018en_US
dc.identifier.citationÖncül, M., Dilsiz, P., Ateş Öz, E., Ateş, T., Aklan, I., Çelik, E. ... Atasoy, D. (2018). Impaired melanocortin pathway function in prader-willi syndrome gene-magel2 deficient mice. Human Molecular Genetics, 27(18), 3129-3136. https://dx.doi.org/10.1093/hmg/ddy216en_US
dc.identifier.issn0964-6906
dc.identifier.issn1460-2083
dc.identifier.urihttps://dx.doi.org/10.1093/hmg/ddy216
dc.identifier.urihttps://hdl.handle.net/20.500.12511/1915
dc.descriptionWOS: 000444203500001en_US
dc.descriptionPubMed ID: 29878108en_US
dc.description.abstractPrader-Willi Syndrome (PWS) is a neurodevelopmental disorder causing social and learning deficits, impaired satiety and severe childhood obesity. Genetic underpinning of PWS involves deletion of a chromosomal region with several genes, including MAGEL2, which is abundantly expressed in the hypothalamus. Of appetite regulating hypothalamic cell types, both AGRP and POMC-expressing neurons contain Magel2 transcripts but the functional impact of its deletion on these cells has not been fully characterized. Here, we investigated these key neurons in Magel2-nullmice in terms of the activity levels at different energy states as well as their behavioral function. Using cell type specific ex vivo electrophysiological recordings and in vivo chemogenetic activation approaches we evaluated impact of Magel2 deletion on AGRP and POMC-neuron induced changes in appetite. Our results suggest that POMC neuron activity profile as well as its communication with downstream targets is significantly compromised, while AGRP neuron function with respect to short term feeding is relatively unaffected in Magel2 deficiency.en_US
dc.description.sponsorshipEuropean Molecular Biology Organisation (EMBO) Installation Grant [2539]en_US
dc.description.sponsorshipThis work was supported by European Molecular Biology Organisation (EMBO) Installation Grant to D.A., grant no. 2539.en_US
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectPrader-Willi Syndromeen_US
dc.subjectObesityen_US
dc.subjectPWS Patientsen_US
dc.titleImpaired melanocortin pathway function in prader-willi syndrome gene-magel2 deficient miceen_US
dc.typearticleen_US
dc.relation.ispartofHuman Molecular Geneticsen_US
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)en_US
dc.authorid0000-0003-4604-4765en_US
dc.authorid0000-0002-3247-613Xen_US
dc.authorid0000-0002-3325-8820en_US
dc.identifier.volume27en_US
dc.identifier.issue18en_US
dc.identifier.startpage3129en_US
dc.identifier.endpage3136en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1093/hmg/ddy216en_US
dc.identifier.wosqualityQ1en_US
dc.identifier.scopusqualityQ1en_US


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