Impaired melanocortin pathway function in prader-willi syndrome gene-magel2 deficient mice

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dc.authorid0000-0003-4604-4765
dc.authorid0000-0002-3247-613X
dc.authorid0000-0002-3325-8820
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.issued2018
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.descriptionWOS: 000444203500001
dc.descriptionPubMed ID: 29878108
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.
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.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/ddy216
dc.identifier.doi10.1093/hmg/ddy216
dc.identifier.endpage3136
dc.identifier.issn0964-6906
dc.identifier.issn1460-2083
dc.identifier.issue18
dc.identifier.scopusqualityQ1
dc.identifier.startpage3129
dc.identifier.urihttps://dx.doi.org/10.1093/hmg/ddy216
dc.identifier.urihttps://hdl.handle.net/20.500.12511/1915
dc.identifier.volume27
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherOxford University Press
dc.relation.ispartofHuman Molecular Geneticsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectPrader-Willi Syndrome
dc.subjectObesity
dc.subjectPWS Patients
dc.titleImpaired melanocortin pathway function in prader-willi syndrome gene-magel2 deficient mice
dc.typeArticle

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