ArticleThe Journal of biological chemistry2013
Gene knockout using transcription activator-like effector nucleases (TALENs) reveals that human NDUFA9 protein is essential for stabilizing the junction between membrane and matrix arms of complex I.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- YY1-mediated NDUFA9 upregulation promotes NSCLC cell growth through mitochondrial and Akt-mTOR pathway modulation.Cell death & disease · 2026Article
- Complex II assembly drives metabolic adaptation to OXPHOS dysfunction.Science advances · 2025Article
- A multi-omics prognostic model of cuproptosis affects the prognosis of stomach adenocarcinoma.Clinical epigenetics · 2025Article
- Integrated bioinformatics and experiment validation reveal cuproptosis-related biomarkers and therapeutic targets in sepsis-induced myocardial dysfunction.BMC infectious diseases · 2025Article
- BiallelicBrain communications · 2025Article
- node2vec2rank: Large Scale and Stable Graph Differential Analysis via Multi-Layer Node Embeddings and Ranking.bioRxiv : the preprint server for biology · 2024Article
- PGC-1s shape epidermal physiology by modulating keratinocyte proliferation and terminal differentiation.iScience · 2023Article
- Conformational changes in mitochondrial complex I of the thermophilic eukaryoteScience advances · 2022Article
- The Combination of ΔCancers · 2022Article
- The coupling mechanism of mammalian mitochondrial complex I.Nature structural & molecular biology · 2022Article
- Applying Sodium Carbonate Extraction Mass Spectrometry to Investigate Defects in the Mitochondrial Respiratory Chain.Frontiers in cell and developmental biology · 2022Article
- Optic atrophy-associated TMEM126A is an assembly factor for the ND4-module of mitochondrial complex I.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- C9orf72 regulates energy homeostasis by stabilizing mitochondrial complex I assembly.Cell metabolism · 2021Article
- Fatal perinatal mitochondrial cardiac failure caused by recurrentMed (New York, N.Y.) · 2021Article
- The Mysterious Multitude: Structural Perspective on the Accessory Subunits of Respiratory Complex I.Frontiers in molecular biosciences · 2021Review
- Analysis of Human Mutations in the Supernumerary Subunits of Complex I.Life (Basel, Switzerland) · 2020Review
- Low abundance of NDUFV2 and NDUFS4 subunits of the hydrophilic complex I domain and VDAC1 predicts mammalian longevity.Redox biology · 2020Article
- Mitochondrial supercomplex assembly promotes breast and endometrial tumorigenesis by metabolic alterations and enhanced hypoxia tolerance.Nature communications · 2019Article
- Knockout ofAnimal models and experimental medicine · 2019Article
- Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease.Molecular brain · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription activator-like effector nucleases (TALENs) represent a promising approach for targeted knock-out of genes in cultured human cells. We used TALEN-technology to knock out the nuclear gene encoding NDUFA9, a subunit of mitochondrial respiratory chain complex I in HEK293T cells. Screening for the knock-out revealed a mixture of NDUFA9 cell clones that harbored partial deletions of the mitochondrial N-terminal targeting signal but were still capable of import. A cell line lacking functional copies of both NDUFA9 alleles resulted in a loss of NDUFA9 protein expression, impaired assembly of complex I, and cells incapable of growth in galactose medium. Cells lacking NDUFA9 contained a complex I subcomplex consisting of membrane arm subunits but not marker subunits of the matrix arm. Re-expression of NDUFA9 restored the defects in complex I assembly. We conclude that NDUFA9 is involved in stabilizing the junction between membrane and matrix arms of complex I, a late assembly step critical for complex I biogenesis and activity.
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