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Adaptation of respiratory chain biogenesis to cytochrome c oxidase deficiency caused by SURF1 gene mutations

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    SYSNO ASEP0383276
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleAdaptation of respiratory chain biogenesis to cytochrome c oxidase deficiency caused by SURF1 gene mutations
    Author(s) Kovářová, Nikola (FGU-C) RID
    Vrbacká-Čížková, Alena (FGU-C)
    Pecina, Petr (FGU-C) RID, ORCID
    Stránecký, V. (CZ)
    Pronicka, E. (PL)
    Kmoch, S. (CZ)
    Houštěk, Josef (FGU-C) RID, ORCID
    Source TitleBiochimica Et Biophysica Acta-Molecular Basis of Disease. - : Elsevier - ISSN 0925-4439
    Roč. 1822, č. 7 (2012), s. 1114-1124
    Number of pages11 s.
    Languageeng - English
    CountryNL - Netherlands
    Keywordsmitochondrial disorder ; SURF1 gene ; Leigh syndrome ; gene expression ; oxidative phosphorylation ; cytochrome c oxidase
    Subject RIVFG - Pediatrics
    R&D ProjectsNS9759 GA MZd - Ministry of Health (MZ)
    NT12370 GA MZd - Ministry of Health (MZ)
    GD305/08/H037 GA ČR - Czech Science Foundation (CSF)
    Institutional supportFGU-C - RVO:67985823
    CEZAV0Z50110509 - FGU-C (2005-2011)
    UT WOS000304727500005
    DOI10.1016/j.bbadis.2012.03.007
    AnnotationSURF1 gene mutations are frequent cause of severe assembly defects of cytochrome c oxidase (COX) with clinical manifestation of Leigh syndrome. In this study, fibroblasts cell lines from patients with different SURF1 mutations were analyzed to investigate changes in protein and transcript levels of OXPHOS complexes and other pro-mitochondrial genes due to SURF1 mutations. Immunoblott analysis revealed decreased amount of COX accompanied by compensatory increase of respiratory chain complexes I, III and V. Altered biogenesis of COX resulted in accumulation of COX assembly intermediates. In patient cells the residual COX was incorporated predominantly into I-III2-IV1 supercomplex. Whole genome expression profiling showed general decrease of transcriptional activity in patients cells and indicated that observed compensatory changes in OXPHOS complexes originate from posttranscriptional mechanisms
    WorkplaceInstitute of Physiology
    ContactLucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400
    Year of Publishing2013
Number of the records: 1  

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