Number of the records: 1  

Mitochondrial localization of human frataxin is necessary but processing is not for rescuing frataxin deficiency in Trypanosoma brucei

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    SYSNO ASEP0318331
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleMitochondrial localization of human frataxin is necessary but processing is not for rescuing frataxin deficiency in Trypanosoma brucei
    TitleMitochondriální lokalizace ale ne procesování lidského frataxinu jsou esenciální pro záchranu frataxinové deficiente u Trypanosoma brucei
    Author(s) Long, Shaojun (BC-A)
    Jirků, Milan (BC-A) RID
    Ayala, F. J. (US)
    Lukeš, Julius (BC-A) RID, ORCID
    Number of authors4
    Source TitleProceedings of the National Academy of Sciences of the United States of America. - : National Academy of Sciences - ISSN 0027-8424
    Roč. 105, č. 36 (2008), s. 13468-13473
    Number of pages6 s.
    Languageeng - English
    CountryUS - United States
    Keywordsfrataxin ; mitochondrion ; Trypanosoma ; Kinetoplastida
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsIAA500960705 GA AV ČR - Academy of Sciences of the Czech Republic (AV ČR)
    LC07032 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    2B06129 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    GA204/06/1558 GA ČR - Czech Science Foundation (CSF)
    CEZAV0Z60220518 - PAU-O, BC-A (2005-2011)
    UT WOS000259251700053
    DOI10.1073/pnas.0806762105
    AnnotationTrypanosoma brucei is the most genetically tractable representative of the domain Excavata and also the causative agent of human sleeping sickness and ruminant nagana. We have attempted to rescue the T. brucei cells with down-regulated frataxin using the human frataxin, the defects of which result in Friedriech’s ataxia. Despite the evolutionary distance between humans and trypanosomes, human frataxin was not only efficiently imported into the T. brucei mitochondrion via its long genuine import signal, but also successfully rescued the phenotype. The rescue was, however, fully dependent on mitochondrial localization of human frataxin.
    WorkplaceBiology Centre (since 2006)
    ContactDana Hypšová, eje@eje.cz, Tel.: 387 775 214
    Year of Publishing2009
Number of the records: 1  

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