Affinage

MIEF1

Mitochondrial ribosome and complex I assembly factor AltMIEF1 · UniProt L0R8F8

Length
70 aa
Mass
8.4 kDa
Annotated
2026-06-10
47 papers in source corpus 19 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/10 claims corpus-supported (90%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MIEF1 (MiD51) is an outer mitochondrial membrane receptor that directly recruits the cytosolic GTPase Drp1 to the mitochondrial surface, governing the balance between mitochondrial fission and fusion (PMID:21701560, PMID:21508961). It functions independently of the other Drp1 receptors Fis1 and Mff, acting as an autonomous recruitment platform whose retargeting to peroxisomes or lysosomes is sufficient to draw Drp1 to those organelles (PMID:23283981, PMID:23921378). Recruitment alone is not activation: its cytosolic domain adopts a catalytically dead nucleotidyltransferase fold that recruits Drp1 through a separate surface loop, while bound nucleotide cofactor is required to convert recruited Drp1 into a fission-competent state — purified MiD51 inhibits Drp1 assembly and GTP hydrolysis, and ADP relieves this inhibition to promote assembly into active spirals (PMID:24515348, PMID:24508339). Long-chain acyl-CoA occupies the same nucleotide-binding pocket and activates MiD51 by inducing its oligomerization, coupling lipid metabolic state to Drp1 GTPase stimulation (PMID:38594588). MIEFs further serve as a platform that hands off Drp1 to Mff and broaden the range of Drp1 oligomeric states engaged during fission (PMID:34805137). Fis1 binds MiD51 directly and can competitively displace Drp1 to further activate fission, particularly under apoptotic stress (PMID:26432782, PMID:38192411). Mechanical cues feed into this machinery: actomyosin tension drives MIEF1 phosphorylation that limits Drp1 recruitment, and MIEF1/Drp1-dependent fission is required to control YAP/TAZ, SREBP, and NRF2 transcriptional programs governing proliferation, lipogenesis, and antioxidant metabolism (PMID:39433949). Loss of MIEF1 sensitizes cells to intrinsic apoptosis and PINK1/PRKN-dependent mitophagy (PMID:30894073). Dominant heterozygous MIEF1 mutations that preserve localization and oligomerization but disrupt mitochondrial network dynamics cause human optic neuropathy (PMID:33632269). A distinct small ORF in the MIEF1 transcript encodes MIEF1-MP, a mitochondrial matrix microprotein that associates with the mitoribosome and stimulates mitochondrial translation (PMID:30215512).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2011 High

    Establishing that mitochondria possess a dedicated Drp1 receptor answered how the fission GTPase is targeted to the organelle surface, identifying MIEF1 as that anchor.

    Evidence Immunofluorescence, reciprocal Co-IP, and knockdown/overexpression in mammalian cells

    PMID:21508961 PMID:21701560

    Open questions at the time
    • Did not resolve whether recruitment alone drives fission or requires additional activation
    • Relationship to existing receptors Fis1/Mff unmapped at this stage
  2. 2011 High

    Showing MIEF1 recruits Drp1 yet inhibits its fission activity revealed a paradoxical receptor that can promote fusion, distinguishing recruitment from activation.

    Evidence Co-IP, overexpression/knockdown with morphology readout, interaction mapping against Mff/hFis1/Mfn2

    PMID:21701560

    Open questions at the time
    • Molecular basis of the inhibitory activity unknown
    • Dose-dependence of fusion vs fission phenotype unresolved
  3. 2013 High

    Genetic null cell lines settled whether MIEF1 acts independently of Fis1 and Mff, confirming it is a bona fide autonomous Drp1 receptor.

    Evidence Fis1-null, Mff-null, and double-null cells with Drp1 puncta imaging; organelle-retargeting constructs

    PMID:23283981 PMID:23921378

    Open questions at the time
    • How the receptors functionally divide labor in normal cells not fully defined
    • Mechanism of MiD51-specific organelle targeting (not peroxisomal) unexplained
  4. 2014 High

    Crystal structures and in vitro reconstitution defined the cytosolic domain as a catalytically dead nucleotidyltransferase fold and identified bound nucleotide as an essential activation cofactor, mechanistically separating Drp1 recruitment from Drp1 activation.

    Evidence X-ray crystallography, site-directed mutagenesis, in vitro Drp1 GTPase and sedimentation/assembly assays

    PMID:24508339 PMID:24515348

    Open questions at the time
    • Physiological identity and dynamics of the bound nucleotide in cells unclear
    • Whether nucleotide occupancy is regulated by metabolic state not addressed
  5. 2016 High

    Combining CRISPR knockouts with proximity labeling and GTPase assays placed MIEF1 in functional opposition to Mff and tied it to apoptotic resistance, clarifying receptor crosstalk.

    Evidence CRISPR knockouts, BioID proximity labeling, Drp1 GTPase assay, apoptosis assays

    PMID:27076521

    Open questions at the time
    • Mechanism by which MiD51 suppresses Mff-driven Drp1 activity not defined
    • Direct vs indirect basis of apoptosis resistance unresolved
  6. 2015 Medium

    Tracking receptor interactions through apoptosis suggested Fis1 competitively displaces Drp1 from MiD51 to activate fission, offering a switch mechanism during stress.

    Evidence Co-IP before/after UV irradiation with imaging

    PMID:26432782

    Open questions at the time
    • Competitive displacement model inferred from correlated Co-IP, not direct competition assay
    • Single lab, not reconstituted
  7. 2018 Medium

    Discovery that a small ORF in the MIEF1 transcript encodes a matrix microprotein revealed a second, translation-regulating product of the locus distinct from the membrane fission receptor.

    Evidence APEX2 proximity labeling, mitoribosome interaction assays, gain/loss-of-function with translation readout

    PMID:30215512

    Open questions at the time
    • Molecular mechanism of mitoribosome stimulation unknown
    • Single lab; relationship to MiD51 fission function unexplored
  8. 2018 Medium

    Linking MiD51 to cell cycle progression and microRNA control extended its role beyond morphology to proliferation in disease contexts.

    Evidence siRNA knockdown, flow cytometry, ERK1/2/CDK4 pathway analysis, miRNA profiling in PASMCs

    PMID:29431643

    Open questions at the time
    • Whether cell cycle effect is downstream of fission per se not isolated
    • Single disease cell context
  9. 2019 Medium

    Knockout studies connected MIEF1 loss to apoptotic priming and PINK1/PRKN mitophagy, defining its contribution to mitochondrial quality control and survival.

    Evidence MIEF1 KO cells, flow cytometry, OCR measurements, PINK1/PRKN pathway analysis, proteasome inhibition

    PMID:30894073

    Open questions at the time
    • Causal order between fission defect, respiration loss, and mitophagy not fully separated
    • Single lab
  10. 2019 Medium

    Mapping two Drp1-binding regions and a dimerization residue refined the structural rules of the MiD51-Drp1 interaction and its dependence on Drp1 nucleotide state.

    Evidence Pull-downs, C452 and Drp1 GTP-binding mutants, morphology assays

    PMID:30703167

    Open questions at the time
    • Stoichiometry of the assembled complex in cells unclear
    • Single lab
  11. 2021 Medium

    In-cell crosslinking showed MIEFs engage a broad range of Drp1 oligomeric states and act as a platform feeding Drp1 to Mff, integrating the two receptors into one assembly pathway.

    Evidence In vivo chemical crosslinking, Mff/MIEF-deficient cells, Drp1 oligomerization mutants, Co-IP

    PMID:34805137

    Open questions at the time
    • Temporal sequence of MIEF-to-Mff handoff not resolved
    • Single lab
  12. 2021 Medium

    Functional characterization of dominant human mutations established MIEF1 as a Mendelian disease gene for optic neuropathy acting through impaired network dynamics rather than mislocalization.

    Evidence Targeted sequencing, high-resolution live imaging, morphology analysis in patient-derived cells

    PMID:33632269

    Open questions at the time
    • Precise molecular defect of the mutant proteins not pinpointed
    • Single lab
  13. 2024 High

    Identifying long-chain acyl-CoA as a pocket-binding activator that drives MiD51 oligomerization linked lipid metabolism directly to Drp1 GTPase stimulation.

    Evidence In vitro GTPase assay, biochemical binding, mutagenesis, cellular rescue with oleic acid treatment

    PMID:38594588

    Open questions at the time
    • In-cell concentrations and regulation of LCACA at the pocket unclear
    • Interplay between ADP and LCACA occupancy not delineated
  14. 2024 High

    Demonstrating that mechanical tension phosphorylates MIEF1 to gate Drp1 recruitment placed mitochondrial fission upstream of mechanoresponsive transcription factors, defining a mechanics-to-metabolism signaling axis.

    Evidence ECM stiffness/force manipulation, mouse skin stretching, phosphorylation assays, DRP1/MIEF loss-of-function, transcription factor readouts

    PMID:39433949

    Open questions at the time
    • Identity of the responsible kinase and phosphosite not fully resolved here
    • Direct link from individual fission events to TF activation incomplete
  15. 2026 Medium

    Identifying MAOA as a direct MIEF1 partner that enhances MIEF1-DRP1 coupling extended the receptor's regulation to oxidative-stress-driven fission in disease tissue.

    Evidence Co-IP, molecular docking and dynamics, MAOA/MIEF1 knockdown/overexpression in trabecular meshwork cells

    PMID:41579974

    Open questions at the time
    • Mechanism by which MAOA enhances coupling unknown
    • Single lab and disease context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple activating inputs to MIEF1 — nucleotide occupancy, acyl-CoA binding, Fis1 competition, mechanical phosphorylation, and partner binding — are integrated to set fission rate in a single cell remains unresolved.
  • No unified model linking cofactor state, phosphorylation, and receptor crosstalk
  • Identity of the mechanoresponsive kinase undefined
  • Relationship between MiD51 fission function and MIEF1-MP translation function unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 1
Localization
GO:0005739 mitochondrion 2
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-162582 Signal Transduction 1
Partners
DNM1LFIS1MAOAMFF

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 MIEF1 (MiD51) is anchored to the outer mitochondrial membrane and directly recruits Drp1 to the mitochondrial surface; knockdown of MIEF1 reduces Drp1 association with mitochondria, leading to unopposed fusion and mitochondrial elongation. Immunofluorescence, co-immunoprecipitation, knockdown/overexpression in mammalian cells The EMBO journal High 21508961 21701560
2011 MIEF1 recruits Drp1 independently of hFis1, Mff, and Mfn2, but inhibits Drp1 fission activity, thereby promoting mitochondrial fusion rather than fission when overexpressed. MIEF1 also interacts with hFis1, and elevated hFis1 partially reverses MIEF1-induced fusion. Co-immunoprecipitation, overexpression and knockdown with mitochondrial morphology readout, interaction mapping with Mff/hFis1/Mfn2 The EMBO journal High 21701560
2013 MiD51 can mediate Drp1 recruitment and mitochondrial fission in the absence of both Fis1 and Mff, demonstrating it acts as an independent Drp1 receptor. Fis1 and Mff regulate the number and size of Drp1 puncta on mitochondria. Fis1-null, Mff-null, and Fis1/Mff double-null cell lines; immunofluorescence analysis of Drp1 puncta Molecular biology of the cell High 23283981
2013 MiD51 overexpression sequesters Drp1 specifically at mitochondria acting as a dominant negative, causing unopposed fusion and peroxisomal elongation. At low-level overexpression forming discrete foci, mitochondrial fission still occurs. Unlike Fis1 and Mff, MiD51 is not targeted to peroxisomes. When MiD51 is artificially targeted to peroxisomes or lysosomes, Drp1 is specifically recruited to those organelles. Overexpression at varying levels, targeting constructs to peroxisomes/lysosomes, immunofluorescence, mitofusin 1/2 double-knockout cells The Journal of biological chemistry High 23921378
2014 Crystal structure of the cytosolic domain of human MiD51 reveals a nucleotidyltransferase fold. MiD51 binds GDP and ADP with high specificity but lacks catalytic transferase residues. Nucleotide-binding mutants still recruit Drp1, but a separate region outside the nucleotidyltransferase fold is required for Drp1 recruitment and foci formation. MiD51 foci depend on Drp1 presence and distribute to daughter organelles after scission. X-ray crystallography, site-directed mutagenesis, pull-down assays, live-cell imaging The Journal of cell biology High 24515348
2014 MiD51 contains a nucleotidyltransferase domain that binds ADP with high affinity. MiD51 recruits Drp1 via a surface loop independently of ADP binding. However, without ADP, recruited Drp1 cannot be activated for fission: purified MiD51 strongly inhibits Drp1 assembly and GTP hydrolysis in vitro, and ADP addition relieves this inhibition and promotes Drp1 assembly into spirals with enhanced GTPase activity. ADP is thus an essential cofactor for MiD51-mediated fission. X-ray crystallography, in vitro GTPase assays, Drp1 sedimentation/assembly assays, mutagenesis Structure High 24508339
2016 MiD51 can suppress Mff-dependent enhancement of Drp1 GTPase activity. Proximity-based biotinylation shows close associations between MiD51, Mff, and Drp1, but not Fis1. Loss of MiD51 and Mff together confers greater mitochondrial connectivity and increased resistance to intrinsic apoptosis than loss of either alone. CRISPR/gene editing knockouts, BioID proximity labeling, Drp1 GTPase activity assay, apoptosis assays Journal of cell science High 27076521
2015 During UV irradiation-induced apoptosis, the interaction between Fis1 and MiD51/MIEF1 increases while the interaction between Drp1 and MiD51/MIEF1 decreases, suggesting that Fis1 competitively binds MiD51 to release and activate Drp1 indirectly. Co-immunoprecipitation before/after UV irradiation, western blotting, immunofluorescence FASEB journal Medium 26432782
2018 MIEF1-MP (MIEF1 microprotein), encoded by a small ORF in the 5'UTR of the MIEF1 transcript, localizes to the mitochondrial matrix and interacts with the mitoribosome. Loss of MIEF1-MP decreases mitochondrial translation rate; elevated MIEF1-MP increases it. APEX2 proximity labeling, ribosome interaction assays, gain/loss-of-function with mitochondrial translation readout Biochemistry Medium 30215512
2019 Loss of MIEF1 triggers translocation of BAX to mitochondria, decreases mitochondrial membrane potential, and promotes release of DIABLO/SMAC and cytochrome c, sensitizing cells to apoptosis. MIEF1 degradation during staurosporine treatment occurs via the ubiquitin-proteasome system. MIEF1 knockout cells, flow cytometry, western blotting, live-cell imaging, proteasome inhibitor experiments Autophagy Medium 30894073
2019 MIEF1 deficiency impairs mitochondrial respiration and induces oxidative stress, sensitizing cells to PINK1-PRKN-mediated mitophagy. Upon MIEF1 loss, PRKN recruitment to depolarized mitochondria leads to UPS-dependent degradation of MFN2 and FIS1. MIEF1 knockout, PINK1/PRKN pathway analysis, oxygen consumption rate measurements, western blotting Autophagy Medium 30894073
2019 Two distinct regions on MiD51 directly bind Drp1; the interaction is regulated by GTP binding to Drp1 and depends on Drp1 polymerization. Dimerization of MiD51 via residue C452 is required for proper regulation of mitochondrial dynamics. Pull-down assays, mutagenesis of MiD51 (C452), Drp1 GTP-binding mutants, mitochondrial morphology assays PloS one Medium 30703167
2021 In intact mammalian cells, Drp1 exists as a mixture of oligomeric assembly states. MIEFs (MIEF1 and MIEF2) bind a wider range of Drp1 assembly states including lower and higher oligomers and recruit both active and inactive Drp1, whereas Mff preferentially binds higher-order Drp1 oligomers and only active forms. MIEFs serve as a platform facilitating Drp1 binding to Mff; loss of MIEFs severely impairs Drp1–Mff interaction. Forced recruitment of Drp1 by MIEFs facilitates Drp1 oligomerization. In vivo chemical crosslinking, Mff/MIEF1/2-deficient cells, Drp1 oligomerization mutants, co-immunoprecipitation Frontiers in cell and developmental biology Medium 34805137
2024 Long-chain acyl-CoA (LCACA) activates MiD51 by inducing its oligomerization, which stimulates Drp1 GTPase activity. LCACA binds in the previously identified nucleotide-binding pocket of MiD51 (1:1 stoichiometry); a point mutation in this pocket reduces LCACA binding and LCACA-induced oligomerization. In cells, the LCACA-binding mutant fails to form puncta or rescue MiD49/51 knockdown effects on mitochondrial length and Drp1 recruitment. MiD51 oligomers synergize with Mff but not actin filaments in Drp1 activation. In vitro Drp1 GTPase assay, biochemical binding assays, site-directed mutagenesis, cell-based rescue experiments, oleic acid treatment Nature cell biology High 38594588
2024 Actomyosin tension promotes phosphorylation of MIEF1, limiting Drp1 recruitment at mitochondria and inhibiting peri-mitochondrial F-actin formation and mitochondrial fission. DRP1- and MIEF1/2-dependent fission is required and sufficient to regulate YAP/TAZ, SREBP1/2, and NRF2 transcription factors in response to mechanical cues, thereby controlling cell proliferation, lipogenesis, antioxidant metabolism, and adipocyte differentiation. ECM stiffness manipulation, applied mechanical forces including mouse skin stretching, phosphorylation assays, DRP1/MIEF1/2 loss-of-function, transcription factor activity readouts Nature cell biology High 39433949
2023 Fis1 and MiD51 engage in a direct protein-protein interaction; peptide inhibitors (CVP-241, CVP-242) disrupt this interaction in vitro with measured binding affinities (Fis1/MiD51 KD 0.054 µM). Disrupting Fis1/MiD51 PPI increases cardiomyocyte viability under hypoxic stress. In vitro binding assays (fluorescence), molecular docking, cell viability assays in H9c2 cardiomyocytes Frontiers in pharmacology Medium 38192411
2026 MAOA interacts directly with MIEF1 (confirmed by co-immunoprecipitation and molecular docking) and enhances MIEF1-DRP1 coupling. Cortisol increases MIEF1 and p-DRP1(Ser616), driving mitochondrial fission; knockdown of MAOA or MIEF1 reduces oxidative stress and mitochondrial fragmentation in trabecular meshwork cells. Co-immunoprecipitation, molecular docking, molecular dynamics simulations, MAOA/MIEF1 knockdown and overexpression, confocal microscopy Free radical biology & medicine Medium 41579974
2021 Dominant heterozygous mutations in MIEF1 do not disrupt MiD51 localization to the outer mitochondrial membrane or its oligomerization, but significantly disrupt mitochondrial network dynamics, causing optic neuropathy in humans. Targeted sequencing, high-resolution confocal live imaging, mitochondrial morphology analysis in patient-derived cells Molecular neurodegeneration Medium 33632269
2018 MiD51 silencing (but not silencing of Fis1 or Mff) causes G1-phase cell cycle arrest through ERK1/2- and CDK4-dependent mechanisms in pulmonary artery smooth muscle cells. MiD upregulation in PAH results from decreased miR-34a-3p expression (epigenetic mechanism). siRNA knockdown, flow cytometry cell cycle analysis, ERK1/2 and CDK4 pathway analysis, microRNA profiling Circulation Medium 29431643
2025 The chromatin remodeler HELLS directly regulates MIEF1 transcription; HELLS knockdown suppresses MIEF1 expression leading to mitochondrial hyperfusion and energy deprivation. The HELLS-MIEF1 axis controls mitochondrial dynamics and genome stability in liver cancer. Loss/gain-of-function experiments (HELLS KD and MIEF1 KD/OE), mitochondrial morphology imaging, ChIP or transcriptional target identification Cell death & disease Medium 40175344

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Fis1, Mff, MiD49, and MiD51 mediate Drp1 recruitment in mitochondrial fission. Molecular biology of the cell 1008 23283981
2011 MiD49 and MiD51, new components of the mitochondrial fission machinery. EMBO reports 518 21508961
2011 Human MIEF1 recruits Drp1 to mitochondrial outer membranes and promotes mitochondrial fusion rather than fission. The EMBO journal 297 21701560
2016 Cooperative and independent roles of the Drp1 adaptors Mff, MiD49 and MiD51 in mitochondrial fission. Journal of cell science 265 27076521
2013 Adaptor proteins MiD49 and MiD51 can act independently of Mff and Fis1 in Drp1 recruitment and are specific for mitochondrial fission. The Journal of biological chemistry 248 23921378
2018 Epigenetic Dysregulation of the Dynamin-Related Protein 1 Binding Partners MiD49 and MiD51 Increases Mitotic Mitochondrial Fission and Promotes Pulmonary Arterial Hypertension: Mechanistic and Therapeutic Implications. Circulation 147 29431643
2015 Drp1, Mff, Fis1, and MiD51 are coordinated to mediate mitochondrial fission during UV irradiation-induced apoptosis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 100 26432782
2016 The role of Drp1 adaptor proteins MiD49 and MiD51 in mitochondrial fission: implications for human disease. Clinical science (London, England : 1979) 98 27660309
2014 Structural and functional analysis of MiD51, a dynamin receptor required for mitochondrial fission. The Journal of cell biology 85 24515348
2018 MIEF1 Microprotein Regulates Mitochondrial Translation. Biochemistry 82 30215512
2014 The mitochondrial fission receptor MiD51 requires ADP as a cofactor. Structure (London, England : 1993) 79 24508339
2000 1,25-Dihydroxyvitamin D3--a hormone with immunomodulatory properties. Zeitschrift fur Rheumatologie 67 10769431
2019 Loss of MIEF1/MiD51 confers susceptibility to BAX-mediated cell death and PINK1-PRKN-dependent mitophagy. Autophagy 55 30894073
2018 The Protein Coded by a Short Open Reading Frame, Not by the Annotated Coding Sequence, Is the Main Gene Product of the Dual-Coding Gene MIEF1. Molecular & cellular proteomics : MCP 48 30181344
2024 Mitochondrial mechanotransduction through MIEF1 coordinates the nuclear response to forces. Nature cell biology 37 39433949
2018 MiD49 and MiD51: New mediators of mitochondrial fission and novel targets for cardioprotection. Conditioning medicine 37 30338314
2019 Matrine promotes apoptosis in SW480 colorectal cancer cells via elevating MIEF1-related mitochondrial division in a manner dependent on LATS2-Hippo pathway. Journal of cellular physiology 32 31119752
2019 Biventricular Increases in Mitochondrial Fission Mediator (MiD51) and Proglycolytic Pyruvate Kinase (PKM2) Isoform in Experimental Group 2 Pulmonary Hypertension-Novel Mitochondrial Abnormalities. Frontiers in cardiovascular medicine 27 30740395
2020 An epigenetic increase in mitochondrial fission by MiD49 and MiD51 regulates the cell cycle in cancer: Diagnostic and therapeutic implications. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 26 32068312
2021 The Molecular Assembly State of Drp1 Controls its Association With the Mitochondrial Recruitment Receptors Mff and MIEF1/2. Frontiers in cell and developmental biology 25 34805137
2024 Fatty acyl-coenzyme A activates mitochondrial division through oligomerization of MiD49 and MiD51. Nature cell biology 20 38594588
2019 New interfaces on MiD51 for Drp1 recruitment and regulation. PloS one 17 30703167
2019 Large tumor suppressor kinase 2 overexpression attenuates 5-FU-resistance in colorectal cancer via activating the JNK-MIEF1-mitochondrial division pathway. Cancer cell international 16 31011291
2019 Melatonin attenuates inflammation-related venous endothelial cells apoptosis through modulating the MST1-MIEF1 pathway. Journal of cellular physiology 15 31169304
2023 Dynamin-Related Protein 1 Binding Partners MiD49 and MiD51 Increased Mitochondrial Fission In Vitro and Atherosclerosis in High-Fat-Diet-Fed ApoE-/- Mice. International journal of molecular sciences 13 38203413
2021 Dominant mutations in MIEF1 affect mitochondrial dynamics and cause a singular late onset optic neuropathy. Molecular neurodegeneration 13 33632269
2019 Yap-Hippo promotes A549 lung cancer cell death via modulating MIEF1-related mitochondrial stress and activating JNK pathway. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 12 30875659
2014 Long-term remission of adenoid cystic tongue carcinoma with low dose naltrexone and vitamin D3--a case report. Oral health and dental management 12 25284545
2019 Mst1 overexpression combined with Yap knockdown augments thyroid carcinoma apoptosis via promoting MIEF1-related mitochondrial fission and activating the JNK pathway. Cancer cell international 11 31139020
2019 MKP1 overexpression reduces TNF-α-induced cardiac injury via suppressing mitochondrial fragmentation and inhibiting the JNK-MIEF1 pathways. Journal of cellular physiology 9 30740674
2023 Ischemia/reperfusion-induced MiD51 upregulation recruits Drp1 to mitochondria and contributes to myocardial injury. Biochemical and biophysical research communications 7 37149986
2023 Selective inhibitors targeting Fis1/Mid51 protein-protein interactions protect against hypoxia-induced damage in cardiomyocytes. Frontiers in pharmacology 7 38192411
2020 MiD51 Is Important for Maintaining Mitochondrial Health in Pancreatic Islet and MIN6 Cells. Frontiers in endocrinology 7 32411091
2022 Valproic acid regulates MIEF1 through MST2-HIPPO to suppress breast cancer growth. Life sciences 6 36126724
2019 Genetic ablation of TAZ induces HepG2 liver cancer cell apoptosis through activating the CaMKII/MIEF1 signaling pathway. OncoTargets and therapy 6 30881030
2025 The Immunogenicity of Coxsackievirus A6 (D3a Sub-Genotype) Virus-Like Particle and mRNA Vaccines. Journal of medical virology 5 39921385
2000 The use of lipiodol and medium chain triglyceride as delivery agents for hepatic arterial administration of 1, 25-dihydroxyvitamin D3--a potential new treatment for hepatocellular carcinoma. Anticancer research 4 10953347
2025 HELLS controls mitochondrial dynamics and genome stability in liver cancer by collusion with MIEF1. Cell death & disease 3 40175344
2025 Knockdown of MiD49 and MiD51 alleviates collagen-induced arthritis and suppresses mitophagy and fatty acid oxidation (FAO) in rheumatoid arthritis fibroblast-like synoviocytes. Free radical biology & medicine 2 40846102
2023 miR-494-5p mediates the antioxidant activity of EPA by targeting the mitochondrial elongation factor 1 gene MIEF1 in HepG2 cells. The Journal of nutritional biochemistry 2 36739098
2020 Mief1 augments thyroid cell dysfunction and apoptosis through inhibiting AMPK-PTEN signaling pathway. Journal of receptor and signal transduction research 1 31960779
2014 Expression, purification, crystallization and preliminary crystallographic study of the cytoplasmic domain of the mitochondrial dynamics protein MiD51. Acta crystallographica. Section F, Structural biology communications 1 24817717
2006 [Vitamin D3--a prodrug of different D3-hormones]. Medizinische Klinik (Munich, Germany : 1983) 1 16826365
2026 Chronic stress-induced steroids mediate mitochondrial fission and fibrosis in the trabecular meshwork via the MIEF1-MAOA complex. Free radical biology & medicine 0 41579974
2026 Mitochondrial Dynamic Proteins MiD49 and MiD51 as Novel Targets of Cardioprotection. Cells 0 41892348
2026 Mitigating Excessive Mitochondrial Fission Through the Development of a Selective Macrocyclic Inhibitor Targeting Fis1/Mid51 Signaling. Journal of medicinal chemistry 0 42175934
2025 A Portrait of Three Mammalian Bicistronic mRNA Transcripts, Derived from the Genes ASNSD1, SLC35A4, and MIEF1. Biochemistry. Biokhimiia 0 40058972

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