Počet záznamů: 1
Mitochondrial translation is the primary determinant of secondary mitochondrial complex I deficiencies.
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SYSNO ASEP 0605191 Druh ASEP A - Abstrakt Zařazení RIV O - Ostatní Název Mitochondrial translation is the primary determinant of secondary mitochondrial complex I deficiencies. Tvůrce(i) Čunátová, Kristýna (FGU-C) RID, ORCID
Vrbacký, Marek (FGU-C) RID, ORCID
Puertas-Frias, Guillermo (FGU-C) RID, ORCID
Alán, Lukáš (FGU-C) RID, ORCID
Vanišová, M. (CZ)
Saucedo-Rodríguez, María José (FGU-C) RID
Houštěk, Josef (FGU-C) RID, ORCID
Fernández-Vizarra, E. (IT)
Neužil, Jiří (BTO-N) RID, ORCID
Pecinová, Alena (FGU-C) RID, ORCID, SAI
Pecina, Petr (FGU-C) RID, ORCID
Mráček, Tomáš (FGU-C) RID, ORCIDZdroj.dok. RedoXplore
Roč. 1, č. 1 (2024)Poč.str. 1 s. Akce International Congress :REDOX BIOLOGY: A Paradigm of the Foundation of Life /5./ Datum konání 27.09.2024 - 29.09.2024 Místo konání Belgrade Země RS - Srbsko Typ akce WRD Jazyk dok. eng - angličtina Země vyd. RS - Srbsko Klíč. slova oxidative phosphorylation system (OXPHOS) ; ATP synthase ; biogenesis ; mitochondria Obor OECD Endocrinology and metabolism (including diabetes, hormones) CEP LX22NPO5104 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy Institucionální podpora FGU-C - RVO:67985823 ; BTO-N - RVO:86652036 DOI https://doi.org/10.70200/RX202401046C Anotace Individual complexes of the mitochondrial oxidative phosphorylation system (OXPHOS) are not linked solely by their function, they also share dependencies at the maintenance/assembly level, where one complex depends on the presence of a different individual complex. Despite the relevance of this “interdependence” behavior for mitochondrial diseases, its true nature remains elusive. To understand the mechanism that can explain this phenomenon, we examined the consequences of the aberration of different OXPHOS complexes in human cells. We demonstrate here that the complete disruption of each of the OXPHOS complexes resulted in a decrease in the complex I (cI) level and that the major reason for this is linked to the downregulation of mitochondrial ribosomal proteins. We conclude that the secondary cI defect is due to mitochondrial protein synthesis attenuation, while the responsible signaling pathways could differ based on the origin of the OXPHOS defect. Pracoviště Fyziologický ústav Kontakt Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Rok sběru 2025 Elektronická adresa https://doi.org/10.70200/RX202401046C
Počet záznamů: 1