Mitochondrial translation is the primary determinant of secondary mitochondrial complex I deficiencies
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00598238" target="_blank" >RIV/67985823:_____/24:00598238 - isvavai.cz</a>
Alternative codes found
RIV/86652036:_____/24:00598238 RIV/00216208:11310/24:10486380 RIV/00064165:_____/24:10486380 RIV/00216208:11110/24:10486380
Result on the web
<a href="https://doi.org/10.1016/j.isci.2024.110560" target="_blank" >https://doi.org/10.1016/j.isci.2024.110560</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.isci.2024.110560" target="_blank" >10.1016/j.isci.2024.110560</a>
Alternative languages
Result language
angličtina
Original language name
Mitochondrial translation is the primary determinant of secondary mitochondrial complex I deficiencies
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30202 - Endocrinology and metabolism (including diabetes, hormones)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2024
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
iScience
ISSN
2589-0042
e-ISSN
2589-0042
Volume of the periodical
27
Issue of the periodical within the volume
8
Country of publishing house
US - UNITED STATES
Number of pages
22
Pages from-to
110560
UT code for WoS article
001285662900001
EID of the result in the Scopus database
2-s2.0-85199960580