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  A Novel Mecp2(Y120D) Knock-in Model Displays Similar Behavioral Traits But Distinct Molecular Features Compared to the Mecp2-Null Mouse Implying Precision Medicine for the Treatment of Rett Syndrome

Gandaglia, A., Brivio, E., Carli, S., Palmieri, M., Bedogni, F., Stefanelli, G., et al. (2019). A Novel Mecp2(Y120D) Knock-in Model Displays Similar Behavioral Traits But Distinct Molecular Features Compared to the Mecp2-Null Mouse Implying Precision Medicine for the Treatment of Rett Syndrome. Molecular Neurobiology, 56(7), 4838-4854. doi:10.1007/s12035-018-1412-2.

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Datensatz-Permalink: https://hdl.handle.net/21.11116/0000-0005-FFA5-2 Versions-Permalink: https://hdl.handle.net/21.11116/0000-0005-FFA6-1
Genre: Zeitschriftenartikel

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 Urheber:
Gandaglia, Anna, Autor
Brivio, Elena1, Autor
Carli, Sara, Autor
Palmieri, Michela, Autor
Bedogni, Francesco, Autor
Stefanelli, Gilda, Autor
Bergo, Anna, Autor
Leva, Barbara, Autor
Cattaneo, Chiara, Autor
Pizzamiglio, Lara, Autor
Cicerone, Marco, Autor
Bianchi, Veronica, Autor
Kilstrup-Nielsen, Charlotte, Autor
D'Annessa, Ilda, Autor
Di Marino, Daniele, Autor
D'Adamo, Patrizia, Autor
Antonucci, Flavia, Autor
Frasca, Angelisa, Autor
Landsberger, Nicoletta, Autor
Affiliations:
1Dept. Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Max Planck Society, Kraepelinstr. 2-10, 80804 Munich, DE, ou_2035294              

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 Zusammenfassung: MeCP2 is a fundamental protein associated with several neurological disorders, including Rett syndrome. It is considered a multifunctional factor with a prominent role in regulating chromatin structure; however, a full comprehension of the consequences of its deficiency is still lacking. Here, we characterize a novel mouse model of Mecp2 bearing the human mutation Y120D, which is localized in the methyl-binding domain. As most models of Mecp2, the Mecp2Y120D mouse develops a severe Rett-like phenotype. This mutation alters the interaction of the protein with chromatin, but surprisingly, it also impairs its association with corepressors independently on the involved interacting domains. These features, which become overt mainly in the mature brain, cause a more accessible and transcriptionally active chromatin structure; conversely, in the Mecp2-null brain, we find a less accessible and transcriptionally inactive chromatin. By demonstrating that different MECP2 mutations can produce concordant neurological phenotypes but discordant molecular features, we highlight the importance of considering personalized approaches for the treatment of Rett syndrome.

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Sprache(n): eng - English
 Datum: 2019-07
 Publikationsstatus: Online veröffentlicht
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: ISI: 000483159700018
DOI: 10.1007/s12035-018-1412-2
 Art des Abschluß: -

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Titel: Molecular Neurobiology
  Andere : Mol. Neurobiol.
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: Clifton, NJ : Humana Press
Seiten: - Band / Heft: 56 (7) Artikelnummer: - Start- / Endseite: 4838 - 4854 Identifikator: ISSN: 0893-7648
CoNE: https://pure.mpg.de/cone/journals/resource/954925558500