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Mitochondrial phenotype in minipig model transgenic for N-terminal part of human mutated huntingtin

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    0485169 - ÚŽFG 2018 CZ eng K - Conference Paper (Czech conference)
    Hansíková, H. - Rodinová, M. - Křížová, J. - Dosoudilová, Z. - Štufková, H. - Bohuslavová, Božena - Klíma, Jiří - Juhás, Štefan - Ellederová, Zdeňka - Motlík, Jan - Zeman, J.
    Mitochondrial phenotype in minipig model transgenic for N-terminal part of human mutated huntingtin.
    The 4th Animal Models of Neurodegenerative Diseases. Liběchov: ÚŽFG AV ČR, v. v. i., 2017, s. 27-28.
    [Animal Models of Neurodegenerative Diseases /4./. Liblice (CZ), 22.10.2017-24.10.2017]
    R&D Projects: GA MŠMT(CZ) LO1609; GA MŠMT 7F14308
    Institutional support: RVO:67985904
    Keywords : minipig model * Huntington´s disease
    OECD category: Neurosciences (including psychophysiology

    Huntington’s disease (HD) is neurodegenerative disorder caused by an abnormal expansion of CAG repeat encoding a polyglutamine tract of huntingtin (htt). It has been postulated that mitochondria dysfunction may play significant role in the pathophysiology of the HD. But it is still not known yet in detail how mitochondria are able to cover energy needs of the cells during the progression of the HD.
    Permanent Link: http://hdl.handle.net/11104/0280242

     
     
Number of the records: 1  

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