ReviewFrontiers in genetics2015
Nuclear gene mutations as the cause of mitochondrial complex III deficiency.
Review in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 145 citations in OpenAlex.
- Melatonin Targets Mitochondrial Redox Homeostasis: Optimizing the Intracellular Microenvironment.International journal of molecular sciences · 2026Review
- Reversible Metabolic and Liver Disease in Complex III Deficiency: Novel Variants Expand the ReportedCells · 2026Article
- Overview of neuroimaging in primary mitochondrial disorders.Pediatric radiology · 2025Review
- Adult Leigh Syndrome Associated with the m.15635T>C Mitochondrial DNA Variant Affecting the CytochromeInternational journal of molecular sciences · 2025Article
- Pathological variants in nuclear genes causing mitochondrial complex III deficiency: An update.Journal of inherited metabolic disease · 2024Review
- The Ubiquinone-Ubiquinol Redox Cycle and Its Clinical Consequences: An Overview.International journal of molecular sciences · 2024Review
- From Beach to the Bedside: Harnessing Mitochondrial Function in Human Diseases Using New Marine-Derived Strategies.International journal of molecular sciences · 2024Review
- Lessons from the deep: mechanisms behind diversification of eukaryotic protein complexes.Biological reviews of the Cambridge Philosophical Society · 2023Article
- Novel pathogenicCold Spring Harbor molecular case studies · 2023Article
- Machine learning reveals common transcriptomic signatures across rat brain and placenta following developmental organophosphate ester exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Longitudinal in vivo metabolic labeling reveals tissue-specific mitochondrial proteome turnover rates and proteins selectively altered by parkin deficiency.Scientific reports · 2023Article
- Drug Drop Test: How to Quickly Identify Potential Therapeutic Compounds for Mitochondrial Diseases Using YeastInternational journal of molecular sciences · 2023Review
- Evaluation of endpoints for the study and diagnosis of mitochondrial toxicity and disease: a narrative review.Mutagenesis · 2023Review
- Knockout of the Complex III subunit Uqcrh causes bioenergetic impairment and cardiac contractile dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- Identification of mitochondrial respiratory chain signature for predicting prognosis and immunotherapy response in stomach adenocarcinoma.Cancer cell international · 2023Article
- Mitochondrial Neurodegeneration: Lessons fromBiomolecules · 2023Review
- Bcs1, a novel target for fungicide.Frontiers in chemistry · 2023Review
- Metabolic collateral lethal target identification reveals MTHFD2 paralogue dependency in ovarian cancer.Nature metabolism · 2022Article
- Clinical and diagnostic characteristics of complex III mitopathy due to novel BCS1L gene mutation in a Saudi patient.BMC medical genomics · 2022Article
- Mitochondrial Neurodegeneration.Cells · 2022Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Complex III (CIII) deficiency is one of the least common oxidative phosphorylation defects associated to mitochondrial disease. CIII constitutes the center of the mitochondrial respiratory chain, as well as a crossroad for several other metabolic pathways. For more than 10 years, of all the potential candidate genes encoding structural subunits and assembly factors, only three were known to be associated to CIII defects in human pathology. Thus, leaving many of these cases unresolved. These first identified genes were MT-CYB, the only CIII subunit encoded in the mitochondrial DNA; BCS1L, encoding an assembly factor, and UQCRB, a nuclear-encoded structural subunit. Nowadays, thanks to the fast progress that has taken place in the last 3-4 years, pathological changes in seven more genes are known to be associated to these conditions. This review will focus on the strategies that have permitted the latest discovery of mutations in factors that are necessary for a correct CIII assembly and activity, in relation with their function. In addition, new data further establishing the molecular role of LYRM7/MZM1L as a chaperone involved in CIII biogenesis are provided.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.