Affinage

MFN1

Mitofusin-1 · UniProt Q8IWA4

Length
741 aa
Mass
84.2 kDa
Annotated
2026-04-28
67 papers in source corpus 21 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MFN1 is a dynamin-related GTPase anchored in the mitochondrial outer membrane that drives mitochondrial fusion through GTP-hydrolysis-dependent conformational cycling and trans-dimerization of its GTPase domains between apposing organelles (PMID:28114303). MFN1 forms both homotypic complexes and heterotypic complexes with MFN2, with a functional asymmetry whereby MFN1 can complement disease-causing MFN2 alleles but not vice versa (PMID:12527753, PMID:17296794). Its fusogenic activity is tuned by post-translational modifications—acetylation (written by TIP60, erased by HDAC6 and SIRT1) modulates its stability and activity, while ubiquitylation by MARCH5 and Parkin targets it for proteasomal degradation—and by direct inhibitory binding of FUNDC2 to the GTPase domain (PMID:25271058, PMID:24722297, PMID:35710796). Beyond mitochondrial fusion, MFN1 participates in ER–mitochondria tethering via REEP5, supports MAVS-dependent innate antiviral signaling, modulates BAK-dependent apoptotic cytochrome c release, and influences metabolic homeostasis including hepatic lipid oxidation and β-cell insulin secretion (PMID:39133213, PMID:20661427, PMID:38583647, PMID:27613809, PMID:35472764).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2003 High

    Establishing that mammalian mitochondrial fusion requires dedicated outer-membrane GTPases resolved how mitochondrial morphology is maintained: MFN1 and MFN2 are each essential, form functional homotypic and heterotypic complexes, and their loss causes fragmentation and loss of membrane potential.

    Evidence Mfn1 and Mfn2 KO MEFs with rescue experiments, live imaging of mitochondrial fusion

    PMID:12527753

    Open questions at the time
    • Relative contribution of homotypic vs heterotypic complexes in vivo not quantified
    • Mechanism of GTP hydrolysis in fusion not yet defined
  2. 2007 High

    Demonstrating that MFN1 can complement CMT2A-linked MFN2 mutants in trans while MFN2 cannot revealed a functional asymmetry between paralogs, establishing MFN1 as the dominant fusogenic subunit in heterotypic complexes.

    Evidence Complementation assays in Mfn-null MEFs, co-immunoprecipitation of heterooligomers

    PMID:17296794

    Open questions at the time
    • Structural basis for paralog asymmetry unknown
    • Whether asymmetry holds in all tissues not tested
  3. 2009 High

    Showing that the BCL-2-family protein CED-9 physically engages FZO-1/Mfn and promotes fusion in a FZO-1- and EAT-3/OPA1-dependent manner linked apoptotic regulators to the mitochondrial fusion machinery.

    Evidence C. elegans in vivo co-IP of CED-9 with FZO-1, genetic epistasis with fzo-1 and eat-3 mutants

    PMID:19704021

    Open questions at the time
    • Direct mammalian BCL-2/MFN1 interaction not fully recapitulated at this point
    • Whether CED-9 activates or simply stabilizes FZO-1 unclear
  4. 2010 Medium

    Identifying MFN1 as a positive regulator of MAVS/IPS-1 aggregation and interferon production expanded MFN1's role beyond fusion to innate antiviral signaling on the mitochondrial outer membrane.

    Evidence MFN1 siRNA knockdown, MAVS redistribution imaging, IFN production assays upon viral challenge

    PMID:20661427

    Open questions at the time
    • Whether MFN1's GTPase activity is required for MAVS signaling untested
    • Physical binding interface between MFN1 and MAVS unmapped
  5. 2014 High

    Discovery that HDAC6 deacetylates MFN1 under glucose starvation to activate fusion, while MARCH5 ubiquitylates acetylated MFN1 (at K491) for degradation, established acetylation as a central regulatory switch controlling MFN1 activity and turnover.

    Evidence Co-IP of MFN1-HDAC6, acetylation-site mutants, ROS assays, HDAC6-KO mouse fasting model; MARCH5-MFN1 co-IP and K491R/Q mutant ubiquitylation assays in KO MEFs

    PMID:24722297 PMID:25271058

    Open questions at the time
    • Full acetylation site map of MFN1 not determined
    • Whether acetylation alters GTPase domain conformation unknown
  6. 2016 High

    Liver-specific Mfn1 deletion revealed that mitochondrial fragmentation paradoxically enhances respiratory capacity and lipid oxidation, protecting against diet-induced insulin resistance, demonstrating tissue-specific metabolic consequences of MFN1 loss.

    Evidence Liver-specific conditional KO mice, electron microscopy, respirometry, insulin tolerance tests

    PMID:27613809

    Open questions at the time
    • How fragmented mitochondria sustain enhanced respiration mechanistically unclear
    • Whether phenotype depends on compensatory MFN2 activity not addressed
  7. 2017 High

    Crystal structures of MFN1 in multiple nucleotide states defined the GTP-hydrolysis-driven conformational cycle: GTP binding promotes GTPase domain dimerization in the transition state through a conserved aspartate trigger, directly coupling catalysis to membrane tethering.

    Evidence X-ray crystallography of engineered MFN1 constructs, active-site mutagenesis, cellular fusion assays

    PMID:28114303

    Open questions at the time
    • Full-length MFN1 structure not solved
    • Lipid membrane context absent from crystallographic constructs
    • How dimerization generates force for membrane merger not resolved
  8. 2017 Medium

    Identification of SLC25A46 as a negative regulator of MFN1/2 oligomerization showed that MFN1 activity is modulated not only by direct post-translational modifications but also by adjacent membrane proteins controlling its oligomeric state.

    Evidence SLC25A46 knockdown, MFN1 oligomerization and stability assays, mitochondrial morphology

    PMID:28057766

    Open questions at the time
    • Direct physical interaction between SLC25A46 and MFN1 not demonstrated
    • Mechanism of oligomerization control unclear
  9. 2017 Medium

    Showing that SIRT1 deacetylates and stabilizes MFN1 while TIP60 acetylates it completed the writer-eraser cycle for MFN1 acetylation, linking hypoxic stress to mitochondrial elongation.

    Evidence SIRT1 KD/OE, in vitro TIP60 acetylation assays, mitochondrial morphology under hypoxia

    PMID:28669827

    Open questions at the time
    • Whether TIP60 and HDAC6 act on the same or overlapping sites not resolved
    • In vivo relevance of SIRT1-MFN1 axis beyond cell culture not shown
  10. 2022 Medium

    Multiple studies converged to show MFN1 integrates diverse signaling inputs: FUNDC2 directly inhibits MFN1 GTPase activity, βIIPKC phosphorylates MFN1 at S86, MFN1 interaction with BAK restrains apoptosis, and STING1 engages MFN1 to promote ferroptosis-associated fusion, revealing MFN1 as a signaling hub on the outer membrane.

    Evidence GTPase activity assays and domain mapping for FUNDC2; co-IP of MFN1-βIIPKC with peptide antagonist; co-IP of MFN1-BAK/OPA1 with KD rescue of apoptosis; co-IP of STING1-MFN1 with KO ferroptosis assays

    PMID:34195205 PMID:35192161 PMID:35710796 PMID:38583647

    Open questions at the time
    • Whether phosphorylation and acetylation sites interact allosterically unknown
    • Structural basis for FUNDC2 inhibition of GTPase domain unresolved
    • MFN1-BAK findings limited to tamoxifen-resistant breast cancer context
  11. 2022 High

    β-cell-specific double KO of Mfn1/Mfn2 demonstrated that mitofusin-dependent fusion is required for glucose-stimulated ATP production and insulin secretion, a defect bypassable by incretin signaling through cAMP/EPAC.

    Evidence Adult β-cell-selective conditional dKO mice, ATP synthesis, Ca2+ imaging, insulin secretion assays

    PMID:35472764

    Open questions at the time
    • Individual contributions of MFN1 vs MFN2 in β-cells not separated
    • Long-term β-cell survival consequences not assessed
  12. 2022 Medium

    Demonstration that MFN1/2 are enriched at mitochondria-peroxisome contact sites and promote interorganellar clustering extended MFN1's tethering role beyond homotypic mitochondrial fusion.

    Evidence BioID proximity labeling with peroxisomal markers, live-cell imaging, dominant-negative truncation mutant

    PMID:35523862

    Open questions at the time
    • Direct MFN1-peroxisomal receptor interaction not identified
    • Functional consequence of mitochondria-peroxisome tethering on lipid metabolism not tested
  13. 2024 High

    Discovery that REEP5 interacts with MFN1/2 to mediate ER-mitochondria tethering and microtubule-based mitochondrial 'hitchhiking' revealed a mechanism for cytoplasmic distribution of mitochondria coupled to ER dynamics.

    Evidence Reciprocal co-IP (REEP5-MFN1/2), rapamycin-inducible forced dimerization, live-cell imaging, ROS measurements

    PMID:39133213

    Open questions at the time
    • Binding interface between REEP5 and MFN1 unmapped
    • Whether REEP5 modulates MFN1 GTPase activity unknown
  14. 2024 Medium

    Endogenous MFN1 interactome profiling uncovered nutrient-regulated associations with ER, endosomal (RAB5C), and mitochondrial partners, broadening the landscape of MFN1 interorganellar contacts.

    Evidence CRISPR-tagged endogenous MFN1-HA affinity MS, validation of RAB5C, nutrient deprivation conditions

    PMID:39675054

    Open questions at the time
    • Most novel interactors lack functional validation
    • Whether RAB5C-MFN1 interaction is direct or bridged by adaptors untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length MFN1 structure in a membrane context, the force-generating mechanism by which GTPase dimerization drives lipid bilayer merger, and the integrative logic by which acetylation, phosphorylation, and ubiquitylation combinatorially regulate MFN1 activity remain unresolved.
  • No full-length structure of membrane-embedded MFN1
  • Reconstituted fusion assay with purified MFN1 not achieved
  • Combinatorial post-translational modification code not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 3
Localization
GO:0005739 mitochondrion 5 GO:0005886 plasma membrane 2
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 5 R-HSA-5357801 Programmed Cell Death 3 R-HSA-1430728 Metabolism 2 R-HSA-168256 Immune System 1
Partners
BAK1FUNDC2HDAC6MARCH5MAVSMFN2OPA1REEP5
Complex memberships
MFN1 homotypic trans-dimerMFN1-MFN2 heterotypic complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 MFN1 and MFN2 form homotypic and heterotypic complexes on the mitochondrial outer membrane and are essential for mitochondrial fusion; cells lacking Mfn1 or Mfn2 show severely reduced mitochondrial fusion, and homotypic complexes of each mitofusin are functional for fusion. Loss of either causes mitochondrial fragmentation and loss of membrane potential in a subset of mitochondria. Knockout mouse embryonic fibroblasts, rescue experiments with individual Mfn expression, mitochondrial morphology assays (live imaging), membrane potential measurements The Journal of cell biology High 12527753
2007 Wild-type MFN1 can complement CMT2A disease-causing MFN2 mutants through formation of heterooligomeric complexes in trans between mitochondria, restoring fusion activity. Wild-type MFN2 cannot complement the same disease alleles, establishing a functional asymmetry between the two paralogs. Complementation assays in Mfn1/Mfn2 mutant MEFs, co-immunoprecipitation of heterooligomeric complexes, mitochondrial fusion assays The Journal of cell biology High 17296794
2017 Crystal structures of engineered human MFN1 (GTPase domain + helical domain) reveal that GTP binding induces conformational changes promoting GTPase domain dimerization in the transition state. The helical domain resembles the 'neck' of bacterial dynamin-like proteins. A conserved aspartate residue acts as a trigger affecting mitochondrial elongation through GTP-loading-dependent domain rearrangement. Disruption of GTPase domain dimerization abolishes MFN1 fusogenic activity. X-ray crystallography of engineered MFN1 constructs in multiple nucleotide states, active-site mutagenesis, mitochondrial fusion assays in cells Nature High 28114303
2010 MFN1 associates with IPS-1 (MAVS) on the mitochondrial outer membrane and positively regulates RLR-mediated innate antiviral responses. Knockdown of MFN1 abrogates virus-induced redistribution of IPS-1 into speckle-like aggregates and abolishes IFN production. siRNA knockdown of MFN1, immunofluorescence for IPS-1 redistribution, IFN production assays upon viral infection or 5'ppp-RNA transfection PLoS pathogens Medium 20661427
2014 Upon glucose starvation, MFN1 associates with the deacetylase HDAC6, leading to MFN1 deacetylation and activation, which promotes mitochondrial fusion to suppress oxidative stress. HDAC6-deficient cells fail to undergo fusion-induced protection. An acetylation-resistant MFN1 mutant suppresses excess ROS production. In fasting mice, skeletal muscle mitochondria undergo dramatic fusion that is abrogated in HDAC6-knockout animals. Co-immunoprecipitation (MFN1-HDAC6), acetylation-resistant MFN1 mutant rescue, ROS measurements, mitochondrial morphology assays, HDAC6-KO mouse fasting model Journal of cell science High 25271058
2014 MARCH5 E3 ubiquitin ligase binds MFN1 and ubiquitylates it in a manner dependent on MFN1 acetylation at K491; the acetylation-deficient K491R mutant shows weak MARCH5 interaction and reduced ubiquitylation, whereas the acetylation-mimetic K491Q mutant does not. MARCH5-mediated quality control on acetylated MFN1 maintains appropriate MFN1 levels for cell survival under mitochondrial stress. Co-immunoprecipitation (MARCH5-MFN1), acetylation point mutants (K491R, K491Q), ubiquitylation assays, MARCH5-KO MEFs Cell death & disease High 24722297
2017 SIRT1 deacetylase stabilizes MFN1 protein; its knockdown reduces MFN1 levels while SIRT1 overexpression increases them. TIP60 acetyltransferase promotes MFN1 acetylation and reduction, an effect abolished by co-expression of SIRT1. Under hypoxia, SIRT1 and MFN1 accumulate together, driving mitochondrial elongation. In vitro acetylation assays confirm TIP60 acetylates MFN1. siRNA knockdown and overexpression of SIRT1, in vitro acetylation assays, mitochondrial morphology assays under hypoxia Cellular signalling Medium 28669827
2009 In C. elegans, the BCL-2-like protein CED-9 physically interacts with FZO-1 (the Mfn1/2 homologue) in vivo and promotes complete mitochondrial fusion (outer and inner membranes) in an FZO-1/Mfn1,2- and EAT-3/Opa1-dependent manner. Disruption of CED-9's ability to interact with FZO-1 impairs its ability to cause mitochondrial fusion. C. elegans genetics, in vivo co-immunoprecipitation (CED-9 with FZO-1), mitochondrial morphology assays, genetic epistasis with fzo-1 and eat-3 mutants The Journal of cell biology High 19704021
2017 Rapid degradation of SLC25A46 by the ubiquitin-proteasome system (via E3 ligases MULAN and MARCH5, with P97 and proteasome) results in increased stability and oligomerization of MFN1 and MFN2 on the mitochondrial outer membrane, promoting mitochondrial hyperfusion. SLC25A46 thus acts as a regulator of MFN1/2 oligomerization. siRNA knockdown of SLC25A46, protein stability assays, mitochondrial morphology assays, ubiquitylation assays with MULAN and MARCH5 Molecular biology of the cell Medium 28057766
2021 STING1 accumulates in mitochondria upon erastin-induced ferroptosis and binds MFN1/2 to trigger mitochondrial fusion, leading to ROS production and lipid peroxidation. Genetic depletion of MFN1/2 (but not PINK1 or PRKN) reduces pancreatic cancer cell sensitivity to ferroptosis. Co-immunoprecipitation (STING1 with MFN1/2), genetic KO of MFN1/2, ferroptosis assays (lipid peroxidation, cell death), xenograft mouse models Frontiers in cell and developmental biology Medium 34195205
2022 FUNDC2 directly interacts with the GTPase domain of MFN1 via its amino-terminal region, inhibiting MFN1 GTPase activity and outer mitochondrial membrane fusion. Loss of FUNDC2 leads to mitochondrial elongation and reprogrammed cellular metabolism. Co-immunoprecipitation, domain mapping, GTPase activity assay, FUNDC2 knockdown/KO with mitochondrial morphology and metabolic phenotype Nature communications High 35710796
2022 MFN1 and MFN2 promote clustering between mitochondria and peroxisomes and are enriched at the mitochondria-peroxisome interface. Overexpression of MFNs increases mitochondria-peroxisome contacting sites, and a truncated MFN2 lacking the transmembrane region inhibits peroxisome tethering to mitochondria. Proximity labeling (BioID) with peroxisomal proteins, live-cell imaging of co-clustering, truncation mutant expression Communications biology Medium 35523862
2016 Liver-specific deletion of Mfn1 (Mfn1LKO) produces a highly fragmented mitochondrial network coupled with enhanced mitochondrial respiration capacity, preference for lipid oxidation, and increased complex I abundance. Mfn1LKO mice are protected against diet-induced insulin resistance and sensitized to metformin's hypoglycemic effect. Liver-specific conditional KO mice, mitochondrial morphology assays (electron microscopy), oxygen consumption measurements, insulin tolerance tests, metformin treatment Diabetes High 27613809
2022 β-cell-specific double KO of Mfn1 and Mfn2 reduces mitochondrial length, glucose-induced mitochondrial polarization, ATP synthesis, and cytosolic/mitochondrial Ca2+ increases, impairing glucose-stimulated insulin secretion. Incretin/GLP-1 receptor agonists correct defective secretion through enhanced EPAC-dependent cAMP signaling, bypassing the mitochondrial defect. β-cell-selective adult-restricted dKO mice, mitochondrial morphology, ATP synthesis assays, Ca2+ imaging, cAMP sensor (Epac-camps), insulin secretion assays Diabetes High 35472764
2024 REEP5, an ER tubule-shaping protein, interacts with MFN1/2 to mediate mitochondrial 'hitchhiking' on tubular ER along microtubules. REEP5 depletion causes reduced ER-mitochondria tethering and increased perinuclear mitochondrial localization. Forced irreversible REEP5-MFN1/2 interaction via rapamycin-induced dimerization causes mitochondrial hyperfusion. Disruption of this interaction modulates mitochondrial ROS production. Co-immunoprecipitation (REEP5 with MFN1/2), live-cell imaging of mitochondrial distribution, rapamycin-inducible forced dimerization, REEP5 siRNA KD, ROS measurements The Journal of cell biology High 39133213
2016 MARCH5 mediates ubiquitin-dependent degradation of MFN1 in response to tributyltin (TBT) exposure, causing mitochondrial fragmentation. Knockdown of MARCH5 abolishes TBT-induced MFN1 degradation in iPSCs. siRNA knockdown of MARCH5, MFN1 protein level assays, MitoTracker mitochondrial morphology, ATP measurements in human iPSCs Toxicology in vitro Medium 27133438
2022 MFN1 interacts with BAK and with OPA1; in tamoxifen-resistant breast cancer cells, MFN1-BAK interaction is increased restraining BAK activation, while MFN1-OPA1 interaction is reduced due to augmented OPA1 proteolytic cleavage. Knockdown or pharmacological inhibition of MFN1 restores BAK oligomerization, cytochrome c release, and caspase-3/9 activation, re-sensitizing resistant cells to apoptosis. Co-immunoprecipitation (MFN1-MFN2, MFN1-OPA1, MFN1-BAK), siRNA knockdown, pharmacological inhibition, cytochrome c release assay, caspase activity assay, xenograft models Cancer letters Medium 38583647
2024 Cadmium induces Parkin mitochondrial translocation, which promotes ubiquitin-dependent degradation of MFN1 protein, causing mitochondrial fusion disorder and suppressing testosterone synthesis in Leydig cells. Testis-specific Parkin knockdown prevents MFN1 degradation and mitigates testosterone decline. Mito-TEMPO (mtROS inhibitor) blocks Parkin translocation and MFN1 degradation. Parkin testis-specific KD, MFN1 overexpression, ubiquitination assays, mitochondrial morphology, testosterone measurements, Mito-TEMPO treatment in mouse model Journal of hazardous materials Medium 38555669
2024 Endogenous interactome profiling of MFN1-HA (CRISPR-tagged) by mass spectrometry identified novel ER, endosomal, and mitochondrial interactors of MFN1. RAB5C was validated as an endosomal modulator of mitochondrial homeostasis in interaction with MFN1/2. Interactors are regulated by nutrient deprivation. CRISPR-Cas9 endogenous HA-tagging of MFN1, HA-affinity pulldown mass spectrometry, nutrient deprivation conditions, validation of novel interactors Autophagy Medium 39675054
2022 βIIPKC (protein kinase C βII) accumulates on the mitochondrial outer membrane, phosphorylates MFN1 at serine 86, and increases the MFN1-βIIPKC interaction after subarachnoid hemorrhage (SAH). A selective peptide antagonist of MFN1-βIIPKC association (SAMβA) attenuates neuronal injury, mitochondrial dysfunction, and protects Sirt3-dependent antioxidant activity. Co-immunoprecipitation (MFN1-βIIPKC), βIIPKC inhibitor and SAMβA peptide treatment, mitochondrial function assays, Sirt3 siRNA knockdown, in vitro and in vivo SAH models Translational stroke research Medium 35192161
2022 Protodioscin (PD) induces formation of an MFN1-Bak-IP3R complex on mitochondria, facilitating Ca2+ transfer from ER to mitochondria and triggering apoptosis. Downregulation of either MFN1 or Bak reverses PD-induced apoptosis and mitochondrial membrane potential loss. Co-immunoprecipitation (MFN1-Bak-IP3R), siRNA knockdown of MFN1 and Bak, flow cytometry apoptosis assay, mitochondrial membrane potential measurement Journal of hepatocellular carcinoma Medium 35496076
2025 Using time-resolved tmFRET in solution, GTP binding to MFN1 favors the open state (GTPase and HB1 domains far apart), while GDP+Pi results in an equilibrium between open and closed states. The nucleotide-free (apo) state adopts a conformation distinct from all nucleotide-bound states. These solution measurements reveal the full conformational cycle of MFN1 during GTP hydrolysis. Time-resolved transition metal ion FRET (tmFRET) with fluorescent non-canonical amino acid donors and metal ion acceptors, fluorescence lifetime measurements, distance distribution analysis across GDP-, GDP+Pi-, GTP-bound, and apo states bioRxivpreprint Medium
2025 Mitochondrial 'pull-out'—lateral extrusion from pre-existing mitochondrial tubules generating new mitochondrial ends as preferential fusion sites—requires both MFN1 and DRP1, and occurs predominantly at ER-mitochondria contact sites. Pull-out events are stimulated by conditions favoring oxidative phosphorylation. Live-cell imaging, MFN1 and DRP1 KO/KD, ER-mitochondria contact site visualization, metabolic perturbations bioRxivpreprint Low

Source papers

Stage 0 corpus · 67 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development. The Journal of cell biology 2085 12527753
2007 Complementation between mouse Mfn1 and Mfn2 protects mitochondrial fusion defects caused by CMT2A disease mutations. The Journal of cell biology 285 17296794
2017 MFN1 structures reveal nucleotide-triggered dimerization critical for mitochondrial fusion. Nature 256 28114303
2010 Virus-infection or 5'ppp-RNA activates antiviral signal through redistribution of IPS-1 mediated by MFN1. PLoS pathogens 154 20661427
2021 STING1 Promotes Ferroptosis Through MFN1/2-Dependent Mitochondrial Fusion. Frontiers in cell and developmental biology 146 34195205
2019 MFN1-dependent alteration of mitochondrial dynamics drives hepatocellular carcinoma metastasis by glucose metabolic reprogramming. British journal of cancer 128 31819189
2021 The lncRNA Malat1 regulates microvascular function after myocardial infarction in mice via miR-26b-5p/Mfn1 axis-mediated mitochondrial dynamics. Redox biology 126 33667993
2014 MFN1 deacetylation activates adaptive mitochondrial fusion and protects metabolically challenged mitochondria. Journal of cell science 119 25271058
2014 MARCH5-mediated quality control on acetylated Mfn1 facilitates mitochondrial homeostasis and cell survival. Cell death & disease 109 24722297
2020 Denervation drives skeletal muscle atrophy and induces mitochondrial dysfunction, mitophagy and apoptosis via miR-142a-5p/MFN1 axis. Theranostics 106 31938072
2020 Mitochondrial Fusion Via OPA1 and MFN1 Supports Liver Tumor Cell Metabolism and Growth. Cells 90 31947947
2009 The BCL-2-like protein CED-9 of C. elegans promotes FZO-1/Mfn1,2- and EAT-3/Opa1-dependent mitochondrial fusion. The Journal of cell biology 88 19704021
2016 Mfn1 Deficiency in the Liver Protects Against Diet-Induced Insulin Resistance and Enhances the Hypoglycemic Effect of Metformin. Diabetes 69 27613809
2017 Rapid degradation of mutant SLC25A46 by the ubiquitin-proteasome system results in MFN1/2-mediated hyperfusion of mitochondria. Molecular biology of the cell 68 28057766
2022 FUNDC2 promotes liver tumorigenesis by inhibiting MFN1-mediated mitochondrial fusion. Nature communications 62 35710796
2020 Lentinan-functionalized Selenium Nanoparticles target Tumor Cell Mitochondria via TLR4/TRAF3/MFN1 pathway. Theranostics 60 32802180
2017 Mitochondria elongation is mediated through SIRT1-mediated MFN1 stabilization. Cellular signalling 50 28669827
2017 Frameshift Mutations in Repeat Sequences of ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 Genes in Colon Cancers. Pathology oncology research : POR 47 28803425
2022 The MFN1 and MFN2 mitofusins promote clustering between mitochondria and peroxisomes. Communications biology 40 35523862
2020 Apoptotic Effects of Melittin on 4T1 Breast Cancer Cell Line is associated with Up Regulation of Mfn1 and Drp1 mRNA Expression. Anti-cancer agents in medicinal chemistry 40 32072917
2017 Chlorpyrifos inhibits neural induction via Mfn1-mediated mitochondrial dysfunction in human induced pluripotent stem cells. Scientific reports 36 28112198
2020 MFN2 Plays a Distinct Role from MFN1 in Regulating Spermatogonial Differentiation. Stem cell reports 33 32330448
2019 Resveratrol attenuates cerebral ischaemia reperfusion injury via modulating mitochondrial dynamics homeostasis and activating AMPK-Mfn1 pathway. International journal of experimental pathology 32 31867811
2023 Empagliflozin targets Mfn1 and Opa1 to attenuate microglia-mediated neuroinflammation in retinal ischemia and reperfusion injury. Journal of neuroinflammation 30 38082266
2021 miR-20b suppresses mitochondrial dysfunction-mediated apoptosis to alleviate hyperoxia-induced acute lung injury by directly targeting MFN1 and MFN2. Acta biochimica et biophysica Sinica 28 33347533
2014 MicroRNA-19b targets Mfn1 to inhibit Mfn1-induced apoptosis in osteosarcoma cells. Neoplasma 28 24824927
2022 Mitofusins Mfn1 and Mfn2 Are Required to Preserve Glucose- but Not Incretin-Stimulated β-Cell Connectivity and Insulin Secretion. Diabetes 26 35472764
2022 Baicalein suppresses high glucose-induced inflammation and apoptosis in trophoblasts by targeting the miRNA-17-5p-Mfn1/2-NF-κB pathway. Placenta 23 35306433
2018 5-Fluorouracil inhibits neural differentiation via Mfn1/2 reduction in human induced pluripotent stem cells. The Journal of toxicological sciences 21 30518710
2018 Study on the inhibition of Mfn1 by plant-derived miR5338 mediating the treatment of BPH with rape bee pollen. BMC complementary and alternative medicine 20 29382326
2016 Tributyltin induces mitochondrial fission through Mfn1 degradation in human induced pluripotent stem cells. Toxicology in vitro : an international journal published in association with BIBRA 20 27133438
2024 Environmental cadmium inhibits testicular testosterone synthesis via Parkin-dependent MFN1 degradation. Journal of hazardous materials 19 38555669
2019 Inhibition of cAMP/PKA Pathway Protects Optic Nerve Head Astrocytes against Oxidative Stress by Akt/Bax Phosphorylation-Mediated Mfn1/2 Oligomerization. Oxidative medicine and cellular longevity 19 31781352
2012 High expression of Mfn1 promotes early development of bovine SCNT embryos: improvement of mitochondrial membrane potential and oxidative metabolism. Mitochondrion 19 22245982
2022 Lanthanum decreased VAPB-PTPP51, BAP31-FIS1, and MFN2-MFN1 expression of mitochondria-associated membranes and induced abnormal autophagy in rat hippocampus. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 17 35090998
2022 Genipin Attenuates Diabetic Cognitive Impairment by Reducing Lipid Accumulation and Promoting Mitochondrial Fusion via FABP4/Mfn1 Signaling in Microglia. Antioxidants (Basel, Switzerland) 17 36670935
2018 EET enhances renal function in obese mice resulting in restoration of HO-1-Mfn1/2 signaling, and decrease in hypertension through inhibition of sodium chloride co-transporter. Prostaglandins & other lipid mediators 17 29787809
2024 A detailed review of pharmacology of MFN1 (mitofusion-1)-mediated mitochondrial dynamics: Implications for cellular health and diseases. Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society 16 38463181
2024 IRF1-mediated upregulation of PARP12 promotes cartilage degradation by inhibiting PINK1/Parkin dependent mitophagy through ISG15 attenuating ubiquitylation and SUMOylation of MFN1/2. Bone research 16 39465252
2022 Protodioscin Induces Mitochondrial Apoptosis of Human Hepatocellular Carcinoma Cells Through Eliciting ER Stress-Mediated IP3R Targeting Mfn1/Bak Expression. Journal of hepatocellular carcinoma 16 35496076
2023 The immunoproteasome subunit β2i ameliorates myocardial ischemia/reperfusion injury by regulating Parkin-Mfn1/2-mediated mitochondrial fusion. Cellular and molecular life sciences : CMLS 15 37501008
2022 The Mfn1-βIIPKC Interaction Regulates Mitochondrial Dysfunction via Sirt3 Following Experimental Subarachnoid Hemorrhage. Translational stroke research 11 35192161
2021 Mitochondrial Dynamics Related Genes -MFN1, MFN2 and DRP1 Polymorphisms are Associated with Risk of Lung Cancer. Pharmacogenomics and personalized medicine 11 34163214
2024 Dynamic interaction of REEP5-MFN1/2 enables mitochondrial hitchhiking on tubular ER. The Journal of cell biology 10 39133213
2022 Mitoquinone mitigates paraquat-induced A549 lung epithelial cell injury by promoting MFN1/MFN2-mediated mitochondrial fusion. Journal of biochemical and molecular toxicology 10 35686354
2020 Silibinin treatment results in reducing OPA1&MFN1 genes expression in a rat model hepatic ischemia-reperfusion. Molecular biology reports 10 32249375
2021 Associations between OPA1, MFN1, and MFN2 polymorphisms and primary open angle glaucoma in Polish participants of European ancestry. Ophthalmic genetics 9 34425738
2024 Inhibition of MFN1 restores tamoxifen-induced apoptosis in resistant cells by disrupting aberrant mitochondrial fusion dynamics. Cancer letters 8 38583647
2023 MFN1 augmentation prevents retinal degeneration in a Charcot-Marie-Tooth type 2A mouse model. iScience 8 36936780
2015 Correlation between polymorphisms in the MFN1 gene and myopia in Chinese population. International journal of ophthalmology 8 26682159
2019 Pretreatment of bone mesenchymal stem cells with miR181-c facilitates craniofacial defect reconstruction via activating AMPK-Mfn1 signaling pathways. Journal of receptor and signal transduction research 7 31466503
2024 Endogenous interactomes of MFN1 and MFN2 provide novel insights into interorganelle communication and autophagy. Autophagy 6 39675054
2023 LncRNA gadd7 promotes mitochondrial membrane potential decrease and apoptosis of alveolar type II epithelial cells by positively regulating MFN1 in an in vitro model of hyperoxia-induced acute lung injury. European journal of histochemistry : EJH 6 37254890
2021 The relationship between MFN1 copy number variation and growth traits of beef cattle. Gene 6 34864096
2019 Gemini-Based Lipoplexes Complement the Mitochondrial Phenotype in MFN1-Knockout Mouse Embryonic Fibroblasts. Molecular pharmaceutics 5 31609634
2025 Senolysis by GLS1 Inhibition Ameliorates Kidney Aging by Inducing Excessive mPTP Opening Through MFN1. The journals of gerontology. Series A, Biological sciences and medical sciences 4 39697097
2024 Loss of Mfn1 but not Mfn2 enhances adipogenesis. PloS one 2 39739772
2022 Erratum: Lentinan-functionalized Selenium Nanoparticles target Tumor Cell Mitochondria via TLR4/TRAF3/MFN1 pathway: Erratum. Theranostics 2 36438475
2025 Regulation of Mitochondrial Metabolism by Mfn1 Gene Encoding Mitofusin Affects Cellular Proliferation and Histone Modification. Cells 1 40643535
2024 Quercetin Promotes the Repair of Mitochondrial Function in H9c2 Cells Through the miR-92a-3p/Mfn1 Axis. Current pharmaceutical biotechnology 1 38173217
2026 Effect of Hydroxyapatite Nanoparticles on the Ultrastructure, Developmental Competence, and Expression of ZP3, MFN1, and NPM2 in Vitrified Bovine GV Oocytes. Biology 0 41892266
2025 LncRNA FENDRR Inhibits Mitochondrial Apoptosis via TET2-Mediated DNA Demethylation of MFN1 in NSCPO. Oral diseases 0 40714924
2025 Chronic stress-induced downregulation of MFN1 contributes to fatty liver in chickens. Frontiers in veterinary science 0 41078489
2025 MYC affects mitochondrial function in IgA nephropathy by promoting the degradation of MFN1 through HRD1. Immunologic research 0 41240162
2025 KDM6B induces demethylation of H3K27me3 in MFN1 to modulate aberrant mitophagy in sepsis-induced acute lung injury. Scientific reports 0 41361208
2022 Mitochondrial dysfunction caused by targeted deletion of Mfn1 does not result in telomere shortening in oocytes. Zygote (Cambridge, England) 0 35730364
2020 Corrigendum to "Inhibition of cAMP/PKA Pathway Protects Optic Nerve Head Astrocytes against Oxidative Stress by Akt/Bax Phosphorylation-Mediated Mfn1/2 Oligomerization". Oxidative medicine and cellular longevity 0 33082914