ArticleInternational journal of molecular sciences2016
Cell Type-Specific Modulation of Respiratory Chain Supercomplex Organization.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
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- Novel economical, accurate, sensitive, single-cell analytical method for mitochondrial DNA quantification in mtDNA mutation carriers.Journal of assisted reproduction and genetics · 2023Article
- Mitochondrial supercomplex assembly regulates metabolic features and glutamine dependency in mammalian cells.Theranostics · 2023Article
- The assembly, regulation and function of the mitochondrial respiratory chain.Nature reviews. Molecular cell biology · 2022Review
- Regulation and functional role of the electron transport chain supercomplexes.Biochemical Society transactions · 2021Review
- Comparative analysis of CI- and CIV-containing respiratory supercomplexes at single-cell resolution.Cell reports methods · 2021Article
- A Mitochondrial DNA Variant Elevates the Risk of Gallstone Disease by Altering Mitochondrial Function.Cellular and molecular gastroenterology and hepatology · 2021Article
- Assessment of mitochondrial function in metabolic dysfunction-associated fatty liver disease using obese mouse models.Zoological research · 2020Article
- HIGD2A is Required for Assembly of the COX3 Module of Human Mitochondrial Complex IV.Molecular & cellular proteomics : MCP · 2020Article
- Functional role of respiratory supercomplexes in mice: SCAF1 relevance and segmentation of the QScience advances · 2020Article
- Mitochondrial respiratory chain composition and organization in response to changing oxygen levels.Journal of life sciences (Westlake Village, Calif.) · 2020Article
- Systematic analysis of a mitochondrial disease-causing ND6 mutation in mitochondrial deficiency.Molecular genetics & genomic medicine · 2020Article
- Use of in-gel peroxidase assay for cytochromeBiology open · 2020Article
- Mitochondrial Supercomplexes: Physiological Organization and Dysregulation in Age-Related Neurodegenerative Disorders.Frontiers in endocrinology · 2020Review
- Mitochondrial DNA Haplogroup M7 Confers Disability in a Chinese Aging Population.Frontiers in genetics · 2020Article
- Mitochondria in Embryogenesis: An Organellogenesis Perspective.Frontiers in cell and developmental biology · 2019Article
- CytochromeComputational and structural biotechnology journal · 2019Review
- Human COX7A2L Regulates Complex III Biogenesis and Promotes Supercomplex Organization Remodeling without Affecting Mitochondrial Bioenergetics.Cell reports · 2018Article
- Respiratory chain supercomplexes: Structures, function and biogenesis.Seminars in cell & developmental biology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Respiratory chain complexes are organized into large supercomplexes among which supercomplex In + IIIn + IVn is the only one that can directly transfer electrons from NADH to oxygen. Recently, it was reported that the formation of supercomplex In + IIIn + IVn in mice largely depends on their genetic background. However, in this study, we showed that the composition of supercomplex In + IIIn + IVn is well conserved in various mouse and human cell lines. Strikingly, we found that a minimal supercomplex In + IIIn, termed "lowest supercomplex" (LSC) in this study because of its migration at the lowest position close to complex V dimers in blue native polyacrylamide gel electrophoresis, was associated with complex IV to form a supercomplex In + IIIn + IVn in some, but not all of the human and mouse cells. In addition, we observed that the 3697G>A mutation in mitochondrial-encoded NADH dehydrogenase 1 (ND1) in one patient with Leigh's disease specifically affected the assembly of supercomplex In + IIIn + IVn containing LSC, leading to decreased cellular respiration and ATP generation. In conclusion, we showed the existence of LSC In + IIIn + IVn and impairment of this supercomplex causes disease.
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