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Neurological Deficits of an Rps19(Arg67del) Model of Diamond-Blackfan Anaemia

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    SYSNO ASEP0473380
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleNeurological Deficits of an Rps19(Arg67del) Model of Diamond-Blackfan Anaemia
    Author(s) Kubik-Zahorodna, Agnieszka (UMG-J)
    Schuster, Bjorn (UMG-J)
    Kanchev, Ivan (UMG-J) RID
    Sedláček, Radislav (UMG-J) RID
    Number of authors4
    Source TitleFolia Biologica. - : Univerzita Karlova v Praze - ISSN 0015-5500
    Roč. 62, č. 4 (2016), s. 139-147
    Number of pages9 s.
    Languageeng - English
    CountryCZ - Czech Republic
    Keywordsribosomal-protein s19 ; sod1(g93a) mouse model ; huntingtons-disease ; early pathogenesis ; molecular-basis ; axial apraxia ; mutations ; rps19 ; gene ; mice
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsNT14451 GA MZd - Ministry of Health (MZ)
    Institutional supportUMG-J - RVO:68378050
    UT WOS000384769700001
    AnnotationDiamond-Blackfan anaemia is a rare disease caused by insufficient expression of ribosomal proteins and is characterized by erythroid hypoplasia often accompanied by growth retardation, congenital craniofacial and limb abnormalities. In addition, Diamond-Blackfan anaemia patients also exhibit a number of behavioural abnormalities. In this study we describe the behavioural effects observed in a new mouse mutant carrying a targeted single amino acid deletion in the ribosomal protein RPS19. This mutant, created by the deletion of arginine 67 in RPS19, exhibits craniofacial, skeletal, and brain abnormalities, accompanied by various neurobehavioural malfunctions. A battery of behavioural tests revealed a moderate cognitive impairment and neuromuscular dysfunction resulting in profound gait abnormalities. This novel Rps19 mutant shows behavioural phenotypes resembling that of the human Diamond-Blackfan anaemia syndrome, thus creating the possibility to use this mutant as a unique murine model for studying the molecular basis of ribosomal protein deficiencies.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2017
Number of the records: 1  

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