ArticleNature communications2019
Structural insights of human mitofusin-2 into mitochondrial fusion and CMT2A onset.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
What it found
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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
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- SNTB1 gene polymorphisms and risk of high myopia: meta-analysis and single-center validation.Molecular vision · 2025Pooled it
- Higher-order structural organization of mitochondrial metabolism.The Journal of biological chemistry · 2026Review
- Disease-causing MFN2 mutants impair mitochondrial fission dynamics by distinct DRP1 dysregulation.Cell death & disease · 2026Article
- Review
- PMF proteins mediate mitochondrial fusion in Arabidopsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Regulation of mitochondrial biogenesis and energy metabolism in the heart.Chinese medical journal · 2026Review
- Review
- Mechanistic Insights into the Cardioprotective Effects of Mesenchymal Stem Cell-Derived Exosomes in Myocardial Ischemic Injury: A Systematic Review.Pharmaceutics · 2026Review
- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- AAVrh74.tMCK.NT-3 Surrogate Gene Therapy in a Mouse Model of CMT2A.International journal of molecular sciences · 2026Article
- Genetic commonalities between rare subtypes of ALS and CMT: insights into molecular mechanisms of neurodegeneration.Amino acids · 2026Review
- Review
- Mitochondria in Renal Ischemia-Reperfusion Injury: From Mechanisms to Therapeutics.Biomedicines · 2026Review
- Hereditary Polyneuropathies in the Era of Precision Medicine: Genetic Complexity and Emerging Strategies.Genes · 2026Review
- Zika virus infection induces ultrastructural alterations, mitochondrial dysfunction and oxidative stress in human trophoblast HTR-8/SVneo.Frontiers in cellular and infection microbiology · 2026Article
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- Mitofusin 1 in mitochondrial quality control and anti-inflammatory responses in nucleus pulposus cells during disc degeneration.Scientific reports · 2025Article
- A special latch in yeast mitofusin guarantees mitochondrial fusion by stabilizing self-assembly.Nature communications · 2025Article
- Mitofusin agonists enhances long-term engraftment and potency of HSC culturesbioRxiv : the preprint server for biology · 2025Article
40 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
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Mitofusin-2 (MFN2) is a dynamin-like GTPase that plays a central role in regulating mitochondrial fusion and cell metabolism. Mutations in MFN2 cause the neurodegenerative disease Charcot-Marie-Tooth type 2A (CMT2A). The molecular basis underlying the physiological and pathological relevance of MFN2 is unclear. Here, we present crystal structures of truncated human MFN2 in different nucleotide-loading states. Unlike other dynamin superfamily members including MFN1, MFN2 forms sustained dimers even after GTP hydrolysis via the GTPase domain (G) interface, which accounts for its high membrane-tethering efficiency. The biochemical discrepancy between human MFN2 and MFN1 largely derives from a primate-only single amino acid variance. MFN2 and MFN1 can form heterodimers via the G interface in a nucleotide-dependent manner. CMT2A-related mutations, mapping to different functional zones of MFN2, lead to changes in GTP hydrolysis and homo/hetero-association ability. Our study provides fundamental insight into how mitofusins mediate mitochondrial fusion and the ways their disruptions cause disease.
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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.