ArticleProceedings of the National Academy of Sciences of the United States of America2022
Sideroflexin 4 is a complex I assembly factor that interacts with the MCIA complex and is required for the assembly of the ND2 module.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Mitochondrial integrated stress response activation creates a therapeutic vulnerability to MCL-1 inhibition in acute myeloid leukemia.Cell death & disease · 2026Article
- SFXN3 Serves as a Predictive Biomarker for Cisplatin Response and Survival in Head and Neck Squamous Cell Carcinoma.Oncology research · 2026Article
- Neurological manifestations and genotype-phenotype correlations inBrain communications · 2026Article
- Sideroflexins enable mitochondrial transport of polar neutral amino acids.bioRxiv : the preprint server for biology · 2025Article
- Update of the sideroflexin (SLC56) gene family.Human genomics · 2025Review
- Sideroflexin family genes were dysregulated and associated with tumor progression in prostate cancers.Human genomics · 2025Article
- Dynamic changes in lactate-related genes in microglia and their role in immune cell interactions after ischemic stroke.Open medicine (Warsaw, Poland) · 2025Article
- Systematic analysis of NDUFAF6 in complex I assembly and mitochondrial disease.Nature metabolism · 2024Article
- Using cryo-EM to understand the assembly pathway of respiratory complex I.Acta crystallographica. Section D, Structural biology · 2024Article
- Exploring the novel duo of Reticulocalbin, and Sideroflexin as future biomarker candidates for Exacerbated Chronic Obstructive Pulmonary Disease.Clinical proteomics · 2024Article
- Identification and validation of the nicotine metabolism-related signature of bladder cancer by bioinformatics and machine learning.Frontiers in immunology · 2024Article
- Reduced Protein Import via TIM23 SORT Drives Disease Pathology in TIMM50-Associated Mitochondrial Disease.Molecular and cellular biology · 2024Article
- Translation Fidelity and Respiration Deficits in CLPP-Deficient Tissues: Mechanistic Insights from Mitochondrial Complexome Profiling.International journal of molecular sciences · 2023Article
- Comprehensive analysis of the role of SFXN family in breast cancer.Open medicine (Warsaw, Poland) · 2023Article
- Comprehensive Analysis of Sideroflexin 4 in Hepatocellular Carcinoma by Bioinformatics and Experiments.International journal of medical sciences · 2023Article
- Mitochondrial biology and dysfunction in secondary mitochondrial disease.Open biology · 2022Review
- Elevated SFXN2 limits mitochondrial autophagy and increases iron-mediated energy production to promote multiple myeloma cell proliferation.Cell death & disease · 2022Article
- New Players in Neuronal Iron Homeostasis: Insights from CRISPRi Studies.Antioxidants (Basel, Switzerland) · 2022Article
- A High-Throughput Search for SFXN1 Physical Partners Led to the Identification of ATAD3, HSD10 and TIM50.Biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SignificanceMitochondria are double-membraned eukaryotic organelles that house the proteins required for generation of ATP, the energy currency of cells. ATP generation within mitochondria is performed by five multisubunit complexes (complexes I to V), the assembly of which is an intricate process. Mutations in subunits of these complexes, or the suite of proteins that help them assemble, lead to a severe multisystem condition called mitochondrial disease. We show that SFXN4, a protein that causes mitochondrial disease when mutated, assists with the assembly of complex I. This finding explains why mutations in
Indexed as
Identifiers
What OpenQuestion holds
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.