Affinage

MIEF1

Mitochondrial ribosome and complex I assembly factor AltMIEF1 · UniProt L0R8F8

Length
70 aa
Mass
8.4 kDa
Annotated
2026-04-28
46 papers in source corpus 17 papers cited in narrative 17 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MIEF1 (MiD51) is an outer mitochondrial membrane receptor that governs mitochondrial fission by recruiting and regulating the dynamin-related GTPase DRP1, acting as a metabolic and mechanical signaling node. Its cytosolic nucleotidyltransferase-fold domain binds ADP and long-chain acyl-CoA (LCACA); in the ligand-free state MIEF1 sequesters DRP1 and inhibits its GTPase activity, whereas ADP or LCACA binding induces MIEF1 oligomerization that relieves inhibition, promotes DRP1 assembly into fission-competent spirals, and synergizes with Mff (PMID:24508339, PMID:38594588, PMID:34805137). Actomyosin-dependent phosphorylation of MIEF1 limits DRP1 recruitment in response to extracellular matrix stiffness and mechanical forces, coupling mitochondrial fission to YAP/TAZ, SREBP, and NRF2 transcriptional programs that control proliferation, lipogenesis, and antioxidant metabolism (PMID:39433949). The MIEF1 locus additionally encodes a small open reading frame (MIEF1-MP/altMiD51) whose 70-amino-acid microprotein localizes to the mitochondrial matrix, interacts with the mitoribosome, and stimulates mitochondrial translation (PMID:30215512, PMID:30181344). Dominant heterozygous MIEF1 variants cause late-onset optic neuropathy by disrupting mitochondrial network dynamics without abolishing membrane targeting (PMID:33632269).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2011 High

    Before MIEF1 was identified, DRP1 recruitment to mitochondria was attributed to Fis1 and Mff; the discovery that MIEF1 directly recruits DRP1 independently of these receptors established an alternative, parallel recruitment pathway and revealed that overexpression paradoxically inhibits fission.

    Evidence Overexpression/knockdown with Co-IP, subcellular fractionation, and confocal imaging in mammalian cells (two independent labs)

    PMID:21508961 PMID:21701560

    Open questions at the time
    • Structural basis of MIEF1–DRP1 interaction unknown
    • Whether MIEF1 alone is sufficient for fission in vivo unresolved
    • Relationship between MiD49 and MiD51 redundancy not defined
  2. 2013 High

    The question of whether MIEF1/MiD51 and MiD49 can execute DRP1-dependent fission without Fis1 and Mff was answered: genetic elimination of Fis1 and Mff demonstrated that MiD proteins constitute a functionally independent receptor pathway.

    Evidence Fis1/Mff double-knockout cells with immunofluorescence of DRP1 puncta; organelle retargeting of MiD to peroxisomes/lysosomes

    PMID:23283981 PMID:23921378

    Open questions at the time
    • Direct biochemical mechanism by which MIEF1 modulates DRP1 activity unknown
    • Role of nucleotide binding unexplored
  3. 2014 High

    Crystallography resolved a central paradox—how MIEF1 both recruits and inhibits DRP1—by showing that its nucleotidyltransferase-fold domain binds ADP, and that a separate surface loop recruits DRP1; without ADP, MIEF1 inhibits DRP1 assembly and GTPase activity, while ADP binding relieves inhibition and promotes fission-competent DRP1 spirals.

    Evidence X-ray crystallography, nucleotide-binding assays, in vitro reconstitution with purified proteins, mutagenesis

    PMID:24508339 PMID:24515348

    Open questions at the time
    • Identity of the physiological metabolite controlling MIEF1 in cells not established
    • Oligomerization state of MIEF1 and its regulation not defined
  4. 2016 High

    Functional interplay between MIEF1 and Mff was clarified: MIEF1 suppresses Mff-dependent enhancement of DRP1 GTPase activity, and proximity labeling confirmed close association of MIEF1, Mff, and DRP1 in intact cells; loss of MiD49/51 increased resistance to intrinsic apoptosis.

    Evidence BioID proximity labeling, CRISPR knockout, in vitro DRP1 GTPase assay, apoptosis assays

    PMID:27076521

    Open questions at the time
    • How MIEF1 physically integrates with Mff on the same DRP1 oligomer unclear
    • Apoptotic role not distinguished from general fission defect
  5. 2018 High

    A previously unrecognized translational product of the MIEF1 locus—the 70-amino-acid microprotein MIEF1-MP (altMiD51)—was discovered to localize to the mitochondrial matrix, interact with the mitoribosome, and regulate mitochondrial translation, representing a dual-function locus.

    Evidence APEX2 proximity labeling, stable isotope-labeled peptide absolute quantification, knockdown and overexpression with mitochondrial translation assays

    PMID:30181344 PMID:30215512

    Open questions at the time
    • Specific mitoribosome subunit contact site not identified
    • Whether MIEF1-MP affects specific mitochondrial-encoded transcripts unknown
    • Functional coupling between MiD51 and MIEF1-MP products unexamined
  6. 2019 Medium

    MIEF1 loss was shown to perturb mitochondrial homeostasis beyond fission—imbalancing BCL2 family members, causing BAX translocation, cytochrome c release, impaired respiration, and sensitization to PINK1-PRKN mitophagy—linking MIEF1 to mitochondrial quality control.

    Evidence CRISPR knockout, flow cytometry, mitochondrial respiration assay, western blotting, immunofluorescence

    PMID:30894073

    Open questions at the time
    • Whether apoptotic sensitization is a direct effect or secondary to chronic fission imbalance is unclear
    • Single laboratory; independent replication needed
  7. 2021 Medium

    In vivo crosslinking revealed that MIEFs bind a broader range of DRP1 oligomeric states than Mff and serve as platforms facilitating DRP1 oligomerization and subsequent handoff to Mff, resolving how these receptors cooperate hierarchically.

    Evidence In vivo chemical crosslinking, Co-IP with DRP1 oligomerization mutants, Mff/MIEF1/2-deficient cell lines

    PMID:34805137

    Open questions at the time
    • Structural model of the MIEF1-DRP1-Mff ternary complex lacking
    • Stoichiometry of the handoff not determined
  8. 2021 Medium

    Dominant heterozygous MIEF1 variants were linked to late-onset optic neuropathy, establishing the first Mendelian disease association and demonstrating that variants disrupting mitochondrial network dynamics without affecting membrane targeting or oligomerization can cause neurodegeneration.

    Evidence Targeted sequencing in optic neuropathy patients, live confocal imaging of mitochondrial dynamics, oligomerization assays of variant proteins

    PMID:33632269

    Open questions at the time
    • Precise biochemical defect of disease variants (e.g. DRP1 binding affinity) not measured
    • Penetrance and genotype-phenotype correlation require larger cohorts
  9. 2024 High

    Long-chain acyl-CoA was identified as a second endogenous activating ligand of MIEF1, binding the same nucleotide pocket to induce oligomerization and stimulate DRP1 GTPase activity, linking fatty acid metabolism to mitochondrial fission through MiD51.

    Evidence In vitro GTPase and oligomerization assays with purified proteins, point mutagenesis of LCACA-binding site, siRNA rescue, oleic acid cellular treatment

    PMID:38594588

    Open questions at the time
    • Relative contribution of ADP vs. LCACA under physiological conditions unknown
    • Whether other acyl-CoA chain lengths have distinct effects untested
  10. 2024 High

    MIEF1 was established as a mechanotransduction effector: actomyosin tension phosphorylates MIEF1, limiting DRP1 recruitment and fission, and this pathway is necessary and sufficient to regulate YAP/TAZ, SREBP, and NRF2 transcription in response to matrix stiffness.

    Evidence Phosphorylation assays, DRP1/MIEF1/2 KO/KD with transcriptional and metabolic readouts, in vivo mouse skin stretching, genetic epistasis

    PMID:39433949

    Open questions at the time
    • Kinase directly phosphorylating MIEF1 not identified
    • Specific phosphorylation sites and their individual contributions not mapped
    • How mitochondrial fission state is decoded by transcription factors mechanistically unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the identity of the kinase that phosphorylates MIEF1 downstream of actomyosin tension; a structural model of the MIEF1-DRP1-Mff ternary complex; the physiological balance between ADP and LCACA in regulating MIEF1 oligomerization; and whether MIEF1-MP functionally coordinates with MiD51 to integrate mitochondrial translation and dynamics.
  • No kinase identified for mechanotransduction-dependent MIEF1 phosphorylation
  • No ternary structural model of MIEF1-DRP1-Mff
  • Functional interplay between MiD51 and MIEF1-MP gene products untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0060090 molecular adaptor activity 4
Localization
GO:0005739 mitochondrion 5
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 6 R-HSA-5357801 Programmed Cell Death 3 R-HSA-1430728 Metabolism 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-162582 Signal Transduction 1
Partners
DNM1LFIS1MAOAMFFMIEF2

Evidence

Reading pass · 17 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 mitochondria independently of hFis1, Mff, and Mfn2; elevated MIEF1 inhibits Drp1 activity and promotes mitochondrial fusion, while MIEF1 depletion causes fragmentation. MIEF1 also interacts with hFis1, and elevated hFis1 partially reverses MIEF1-induced fusion. Overexpression/knockdown with confocal imaging of mitochondrial morphology, co-immunoprecipitation, subcellular fractionation The EMBO journal High 21701560
2011 MiD49 and MiD51 form foci and rings around mitochondria, directly recruit Drp1 to the mitochondrial surface, and their knockdown reduces Drp1 association leading to unopposed fusion; overexpression sequesters Drp1 and causes fused tubules to associate with actin. Co-immunoprecipitation, siRNA knockdown, overexpression with fluorescence microscopy EMBO reports High 21508961
2013 MiD49 and MiD51 can mediate Drp1 recruitment and mitochondrial fission independently of Fis1 and Mff, as shown in Fis1/Mff double-null cells; Fis1 and Mff regulate the number and size of Drp1 puncta on mitochondria. Genetic knockout (Fis1-null, Mff-null, Fis1/Mff-null cells), immunofluorescence of Drp1 puncta Molecular biology of the cell High 23283981
2013 MiD49/51 overexpression blocks fission by sequestering Drp1 specifically at mitochondria in a dominant-negative manner, causing unopposed fusion requiring mitofusins 1 and 2. MiD49/51 are not targeted to peroxisomes; when artificially targeted to peroxisomes or lysosomes, they specifically recruit Drp1 to those organelles. Overexpression at varying levels, mitofusin 1/2 KO epistasis, organelle retargeting constructs, fluorescence microscopy The Journal of biological chemistry High 23921378
2014 Crystal structure of the cytosolic domain of human MiD51 reveals a nucleotidyltransferase fold that lacks catalytic residues but specifically binds GDP and ADP. A region outside the nucleotidyltransferase fold is required for Drp1 recruitment and assembly of MiD51 into foci. MiD51 foci depend on Drp1 presence and are distributed to daughter organelles after fission. X-ray crystallography, nucleotide-binding assays, mutagenesis, 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, but without nucleotide binding the recruited Drp1 cannot be activated for fission. Purified MiD51 strongly inhibits Drp1 assembly and GTP hydrolysis in the absence of ADP; ADP addition relieves this inhibition and promotes Drp1 assembly into spirals with enhanced GTP hydrolysis. X-ray crystallography, in vitro GTPase assay, Drp1 assembly assay with purified proteins, mutagenesis Structure High 24508339
2016 MiD51 can suppress Mff-dependent enhancement of Drp1 GTPase activity. Proximity-based biotin labeling (BioID) shows close associations between MiD51, Mff, and Drp1, but not Fis1. Loss of MiD49 and MiD51 confers increased resistance to intrinsic apoptotic stimuli. BioID proximity labeling, CRISPR/Cas9 gene editing, in vitro Drp1 GTPase assay, apoptosis assays Journal of cell science High 27076521
2015 During UV-induced apoptosis, the interaction between Drp1 and MiD51/MIEF1 decreases significantly, while interaction between Fis1 and MiD51/MIEF1 increases markedly, suggesting Fis1 competitively binds MiD51/MIEF1 to activate Drp1 indirectly. Phosphorylation of Drp1-Ser637 is essential for its interaction with Mff. Co-immunoprecipitation before and after UV irradiation, phospho-specific antibodies, western blotting FASEB journal Medium 26432782
2018 MIEF1-MP (MIEF1 microprotein), encoded by a small ORF in the 5'UTR of MIEF1 mRNA, localizes to the mitochondrial matrix and interacts with the mitochondrial ribosome (mitoribosome). Loss of MIEF1-MP decreases mitochondrial translation rate; elevated MIEF1-MP increases translation rate. APEX2 proximity labeling, siRNA knockdown, overexpression, mitochondrial translation assay, subcellular fractionation Biochemistry High 30215512
2018 The predominant translational product of the MIEF1 gene in human cells and colon tissue is not the canonical 463 aa MiD51 protein but the small 70 aa alternative ORF protein (altMiD51), as determined by absolute quantification with stable isotope-labeled peptides. Stable isotope-labeled peptide absolute quantification, parallel reaction monitoring mass spectrometry Molecular & cellular proteomics High 30181344
2019 MIEF1 loss triggers imbalance of BCL2 family members on mitochondria, leading to BAX translocation to mitochondria, decreased mitochondrial membrane potential, and release of DIABLO/SMAC and cytochrome c. MIEF1 deficiency also impairs mitochondrial respiration, induces oxidative stress, and sensitizes cells to PINK1-PRKN-mediated mitophagy. Staurosporine-induced MIEF1 degradation occurs via the ubiquitin-proteasome system. CRISPR KO, siRNA knockdown, flow cytometry, western blotting, mitochondrial respiration assay, immunofluorescence Autophagy Medium 30894073
2019 The interaction between Drp1 and MiD51 is regulated by GTP binding and depends on Drp1 polymerization. Two regions on MiD51 directly bind Drp1, and dimerization of MiD51 (dependent on residue C452) is required for mitochondrial dynamics regulation. Co-immunoprecipitation, mutagenesis (C452), GTP-binding assays, fluorescence microscopy PloS one Medium 30703167
2021 In intact mammalian cells, Drp1 exists as a mixture of oligomeric assemblies. Mff preferentially binds higher-order Drp1 oligomers, while MIEFs (MIEF1 and MIEF2) bind a wider range including lower oligomeric states and recruit both active and inactive Drp1 mutants. Forced recruitment of Drp1 to mitochondria by MIEFs facilitates Drp1 oligomerization. MIEFs serve as a platform facilitating Drp1 binding to Mff; loss of MIEFs severely impairs the Drp1-Mff interaction. In vivo chemical crosslinking, co-immunoprecipitation, Drp1 oligomerization mutants, fluorescence microscopy in Mff/MIEF1/2-deficient cells Frontiers in cell and developmental biology Medium 34805137
2024 Long-chain acyl-CoA (LCACA) activates MiD51 by inducing its oligomerization via binding in the nucleotide-binding pocket (confirmed by a point mutation reducing binding and oligomerization). LCACA-induced MiD51 oligomers stimulate DRP1 GTPase activity; a LCACA-binding mutant fails to assemble into mitochondrial puncta or rescue MiD49/51 KD effects. MiD51 oligomers synergize with Mff but not actin filaments in DRP1 activation. Cellular oleic acid treatment promotes mitochondrial fission in an MiD49/51-dependent manner. In vitro GTPase assay, oligomerization assay, point mutagenesis, siRNA knockdown rescue, confocal microscopy, lipid-binding biochemistry Nature cell biology High 38594588
2024 Extracellular matrix stiffness, spatial confinement, and mechanical forces (including mouse skin stretching) regulate mitochondrial dynamics through MIEF1 phosphorylation. Actomyosin tension promotes MIEF1 phosphorylation, limiting DRP1 recruitment to mitochondria and reducing peri-mitochondrial F-actin formation and fission. DRP1- and MIEF1/2-dependent fission is required and sufficient to regulate YAP/TAZ, SREBP1/2, and NRF2 transcription factors, controlling cell proliferation, lipogenesis, antioxidant metabolism, and adipocyte differentiation in response to mechanical cues. Phosphorylation assays, DRP1/MIEF1/2 KO/KD with defined transcriptional and metabolic readouts, in vivo mouse skin stretching, live imaging, genetic epistasis Nature cell biology High 39433949
2021 Dominant heterozygous MIEF1 variants causing late-onset optic neuropathy do not disrupt MiD51 localization to the outer mitochondrial membrane or its oligomerization, but significantly disrupt mitochondrial network dynamics as shown by high-resolution live confocal imaging. Targeted sequencing, live confocal microscopy of mitochondrial dynamics, oligomerization assays in patient-derived variant cells Molecular neurodegeneration Medium 33632269
2026 MAOA (monoamine oxidase A) physically interacts with MIEF1 and enhances MIEF1-DRP1 coupling; cortisol increases both MIEF1 and DRP1-Ser616 phosphorylation, driving excessive mitochondrial fission and trabecular meshwork fibrosis. Knockdown of MAOA or MIEF1 reduces oxidative stress, mitochondrial fragmentation, and extracellular matrix remodeling. Co-immunoprecipitation, molecular docking, molecular dynamics simulations, siRNA knockdown, western blotting, confocal microscopy Free radical biology & medicine Medium 41579974

Source papers

Stage 0 corpus · 46 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 993 23283981
2011 MiD49 and MiD51, new components of the mitochondrial fission machinery. EMBO reports 514 21508961
2011 Human MIEF1 recruits Drp1 to mitochondrial outer membranes and promotes mitochondrial fusion rather than fission. The EMBO journal 296 21701560
2016 Cooperative and independent roles of the Drp1 adaptors Mff, MiD49 and MiD51 in mitochondrial fission. Journal of cell science 263 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 247 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 142 29431643
2016 The role of Drp1 adaptor proteins MiD49 and MiD51 in mitochondrial fission: implications for human disease. Clinical science (London, England : 1979) 98 27660309
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 98 26432782
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 79 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 47 30181344
2018 MiD49 and MiD51: New mediators of mitochondrial fission and novel targets for cardioprotection. Conditioning medicine 36 30338314
2024 Mitochondrial mechanotransduction through MIEF1 coordinates the nuclear response to forces. Nature cell biology 34 39433949
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
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
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 24 32068312
2024 Fatty acyl-coenzyme A activates mitochondrial division through oligomerization of MiD49 and MiD51. Nature cell biology 18 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
2021 Dominant mutations in MIEF1 affect mitochondrial dynamics and cause a singular late onset optic neuropathy. Molecular neurodegeneration 13 33632269
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 12 38203413
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 6 37149986
2023 Selective inhibitors targeting Fis1/Mid51 protein-protein interactions protect against hypoxia-induced damage in cardiomyocytes. Frontiers in pharmacology 6 38192411
2022 Valproic acid regulates MIEF1 through MST2-HIPPO to suppress breast cancer growth. Life sciences 6 36126724
2020 MiD51 Is Important for Maintaining Mitochondrial Health in Pancreatic Islet and MIN6 Cells. Frontiers in endocrinology 6 32411091
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 4 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 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
2025 HELLS controls mitochondrial dynamics and genome stability in liver cancer by collusion with MIEF1. Cell death & disease 1 40175344
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
2025 A Portrait of Three Mammalian Bicistronic mRNA Transcripts, Derived from the Genes ASNSD1, SLC35A4, and MIEF1. Biochemistry. Biokhimiia 0 40058972