Affinage

CISD1

CDGSH iron-sulfur domain-containing protein 1 · UniProt Q9NZ45

Length
108 aa
Mass
12.2 kDa
Annotated
2026-06-09
100 papers in source corpus 46 papers cited in narrative 46 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CISD1/mitoNEET is an integral outer mitochondrial membrane homodimer that coordinates redox-active, pH-labile [2Fe-2S] clusters and functions as a regulated Fe-S cluster donor and redox enzyme controlling mitochondrial iron handling and energy metabolism (PMID:17376863, PMID:17766440, PMID:22961109). Each protomer binds its cluster through a unique 3-Cys/1-His motif (Cys72/Cys74/Cys83/His87), and the solvent-exposed His87 is the linchpin of cluster lability: its protonation triggers cluster release, it electrochemically couples the drug-binding site to the iron center, and it is strictly required for cluster transfer to acceptor proteins (PMID:17584744, PMID:17905743, PMID:19791753, PMID:21788481). Cluster maturation depends on the mitochondrial ISC machinery and augmenter of liver regeneration (ALR), and once oxidized—only the [2Fe-2S]2+ state is transfer-competent—mitoNEET delivers clusters to apo-ferredoxin, repairs oxidatively damaged IRP1/cytosolic aconitase, and transfers clusters to NAF-1/CISD2, while the reduced cluster represents a dormant state reset by the cytosolic Ndor1/anamorsin (CIA) electron-donor complex (PMID:21788481, PMID:25012650, PMID:26887944, PMID:28426722, PMID:28648056). Cluster transfer is gated by an iron-based redox switch and is tuned by NADPH binding (via Asp84) and by reduction through glutathione reductase, FMN, and flavin shuttles, and mitoNEET itself catalyzes electron transfer from FMNH2 to ubiquinone or O2 (PMID:20932062, PMID:22351774, PMID:24403080, PMID:27923678, PMID:28461337). Functionally, mitoNEET restricts mitochondrial matrix iron import—gating VDAC1 in a redox-dependent manner—thereby setting respiratory capacity, ROS production, and intermitochondrial junction formation (PMID:22961109, PMID:28716905, PMID:31527235). Through this control of mitochondrial iron and lipid peroxidation, CISD1 negatively regulates ferroptosis, and pioglitazone—which stabilizes the Fe-N(His87) bond ~10-fold—suppresses iron uptake and lipid peroxidation (PMID:27510639, PMID:33856229). In mitochondrial quality control, CISD1 acts downstream of PINK1: in Pink1/parkin-mutant flies and patient-derived dopaminergic neurons it accumulates as aberrant disulfide-linked, Fe-S-depleted dimers that block mitophagy, and genetic or pharmacological reduction of CISD1 rescues locomotion, lifespan, dopamine, and mitochondrial ultrastructure (PMID:38273330, PMID:39159312). Consistent with these roles, loss of CISD1 causes a Parkinson's-like striatal phenotype and age-dependent cardiac failure (PMID:28880525, PMID:33514783).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2003 High

    Establishing what mitoNEET is required first identifying it as a discrete mitochondrial protein and a direct drug target, which framed all subsequent mechanistic work.

    Evidence Photoaffinity cross-linking with tritiated pioglitazone, MS, and N-terminal sequencing of mitochondrial fractions

    PMID:14570702

    Open questions at the time
    • Did not define molecular function or cofactor
    • Association with beta-oxidation machinery not mechanistically resolved
  2. 2007 High

    Localization, iron content, and a knockout respiratory phenotype defined mitoNEET as an iron-bearing outer-membrane protein controlling mitochondrial respiratory capacity.

    Evidence Bioinformatics, iron quantification, fractionation, and mitoNEET-null mouse respiration assays

    PMID:17376863

    Open questions at the time
    • Molecular basis of respiratory control unresolved
    • Cofactor chemistry not yet defined
  3. 2007 High

    Atomic-resolution structures defined the novel NEET fold and the unusual 3-Cys/1-His [2Fe-2S] coordination, and showed pioglitazone stabilizes the cluster — establishing the structural logic of cluster lability and drug action.

    Evidence Three independent crystal structures (1.5–1.8 Å) with ligand-stability and UV-vis assays

    PMID:17766439 PMID:17766440 PMID:17905743

    Open questions at the time
    • Did not establish in vivo acceptor proteins
    • Functional consequence of cluster release not shown
  4. 2007 High

    Spectroscopy established that the cluster is redox-active and pH-labile with His protonation triggering release, the first mechanistic hypothesis for cluster shuttling/redox function.

    Evidence EPR, optical spectroscopy, MS, and recombinant mutagenesis

    PMID:17584744

    Open questions at the time
    • Physiological acceptor unidentified
    • Whether release reflects transfer or degradation unresolved
  5. 2009 High

    His87 was shown to electrochemically couple the drug-binding site to the Fe-S center, explaining how thiazolidinediones modulate cluster redox state.

    Evidence Protein film voltammetry and resonance Raman with H87C mutant

    PMID:19388667 PMID:19791753

    Open questions at the time
    • Did not establish physiological signal that tunes His87
    • Downstream consequence of potential shift unaddressed
  6. 2010 High

    NADPH binding (K55/H58) and valence-localized cluster characterization linked cellular redox metabolites to cluster stability, indicating regulated release.

    Evidence NMR, ITC, UV-vis, CD, and multifrequency EPR with 15N-labeling

    PMID:20099820 PMID:20932062

    Open questions at the time
    • In vivo relevance of NADPH-driven destabilization not tested
    • Acceptor of released cluster still unknown
  7. 2011 High

    In vitro reconstitution demonstrated unidirectional cluster transfer to apo-ferredoxin requiring His87, defining mitoNEET as a cluster donor and explaining pioglitazone's block of iron transfer.

    Evidence UV-vis, native-PAGE cluster transfer assays, H87C/K55E mutagenesis, cellular mitochondrial iron assays

    PMID:21636891 PMID:21788481

    Open questions at the time
    • Physiological acceptor in cells not yet identified
    • Directionality control mechanism unresolved
  8. 2012 High

    NADPH inhibition of cluster transfer via Asp84, and reciprocal in vivo manipulation showing mitoNEET limits matrix iron import, connected cofactor chemistry to control of respiration and beta-oxidation.

    Evidence In vitro transfer assays with D84 mutants; transgenic overexpression and shRNA knockdown with mitochondrial iron and metabolic readouts

    PMID:22351774 PMID:22961109

    Open questions at the time
    • Transporter coupling iron import to mitoNEET not yet defined
    • Whether iron control is via cluster transfer or membrane gating unresolved
  9. 2014 High

    Genetic epistasis identified the ISC machinery and ALR as mitoNEET's maturation pathway and IRP1/cytosolic aconitase as a physiological cluster acceptor for oxidative repair, placing mitoNEET in iron-sulfur homeostasis.

    Evidence siRNA epistasis of ISC/CIA components, in vitro Fe-S assembly, cluster transfer to IRP1 after nitrosative stress

    PMID:25012650

    Open questions at the time
    • How ALR specifically routes clusters to mitoNEET unresolved
    • In vivo extent of IRP1 repair not quantified
  10. 2014 High

    Identification of glutathione reductase as a physiological reductant and reversible H2O2 oxidation defined the redox systems that toggle mitoNEET between states.

    Evidence In vitro reduction/oxidation assays with multiple reductants, NEM inhibition, UV-vis

    PMID:24403080 PMID:25645953

    Open questions at the time
    • In vivo dominant reductant not established
    • Thioredoxin system explicitly inactive but alternatives untested
  11. 2016 High

    Demonstration that only the oxidized cluster is transfer-competent established an iron-based redox switch governing donor activity, with the reduced state dormant.

    Evidence Controlled spectroscopic redox manipulation and anaerobic cluster transfer assays (UV-vis, EPR)

    PMID:26887944

    Open questions at the time
    • Cellular signal setting the switch unresolved
    • Spatial coupling to acceptor proteins not defined
  12. 2016 High

    mitoNEET was shown to negatively regulate ferroptosis by limiting mitochondrial iron uptake and lipid peroxidation, linking its iron control to a cell-death program.

    Evidence shRNA/siRNA knockdown, pioglitazone treatment, erastin ferroptosis model with iron and lipid peroxidation readouts

    PMID:27510639

    Open questions at the time
    • Downstream lipid peroxidation effectors not defined in this study
    • Whether ferroptosis protection requires cluster transfer unresolved
  13. 2016 Medium

    Identification of FMN as a specific electron shuttle for cluster reduction set up the redox-enzyme model of mitoNEET.

    Evidence EPR, UV-vis, flavin reductase/NADH assay, docking

    PMID:27923678

    Open questions at the time
    • Single-lab finding
    • Physiological FMN source at the outer membrane not established
  14. 2017 High

    mitoNEET was defined as a redox enzyme catalyzing electron transfer from FMNH2 to ubiquinone or O2, with kinetics favoring ubiquinone, integrating it into mitochondrial energy metabolism.

    Evidence Reconstituted electron transfer assays and stopped-flow kinetics with multiple acceptors under anaerobic/aerobic conditions

    PMID:28461337 PMID:29704621

    Open questions at the time
    • In vivo electron acceptor not directly confirmed
    • Relationship between enzyme activity and cluster-donor activity unresolved
  15. 2017 High

    Direct interaction and cluster transfer to NAF-1/CISD2, plus shared iron/ROS pathway, established a functional NEET-protein network, while Ndor1/anamorsin was identified as the reductant resetting the dormant state.

    Evidence Y2H, BiFC, in vitro cluster transfer, shRNA epistasis (CISD2); UV-vis/NMR transient-complex analysis (Ndor1/anamorsin)

    PMID:28426722 PMID:28648056

    Open questions at the time
    • Hierarchy between CISD1 and CISD2 cluster handling unresolved
    • Ndor1/anamorsin interaction shown in vitro only
  16. 2017 High

    Knockout/rescue and gain-of-function revealed mitoNEET shapes mitochondrial network architecture and intermitochondrial junctions, mechanistically linking it to respiration and oxidative resistance.

    Evidence 3D-EM reconstruction, EM quantification, respiration assays in KO/rescue cells with an oxidation-resistant mutant

    PMID:28716905

    Open questions at the time
    • Molecular basis of junction formation unresolved
    • Whether junctions require cluster transfer untested
  17. 2019 High

    Demonstration that oxidized mitoNEET binds and gates VDAC1 at the DIDS-sensitive site provided a direct mechanism for redox-dependent control of mitochondrial metabolite and iron flux.

    Evidence In vitro binding, DIDS inhibitor studies in vitro and in cells, mitochondrial iron accumulation assays

    PMID:31527235

    Open questions at the time
    • Structure of the mitoNEET–VDAC1 interface unknown
    • Quantitative contribution to total metabolite flux unresolved
  18. 2022 Medium

    Pharmacological and genetic inhibition linked mitoNEET to PINK1-Parkin mitophagy, suggesting its activity opposes mitophagic turnover.

    Evidence NL-1/rosiglitazone inhibition, shRNA, mitophagy marker Western blots, lysosome imaging

    PMID:35725011

    Open questions at the time
    • Direction of regulation (inhibition vs accumulation) needed clarification
    • Single cell-type system
  19. 2024 High

    Cross-organism genetics placed CISD1 downstream of PINK1, showing that Fe-S-depleted, disulfide-linked CISD1 dimers are the pathogenic species blocking mitophagy and that reducing CISD1 rescues Pink1/parkin-mutant phenotypes.

    Evidence Drosophila Pink1/parkin genetics, human iPSC and patient dopaminergic neurons, disulfide-dimer characterization, Fe-S-binding-mutant epistasis, NL-1/rosiglitazone pharmacology

    PMID:38273330 PMID:39159312

    Open questions at the time
    • Mechanism by which iron-depleted dimers block mitophagy unresolved
    • Whether the pathogenic dimer forms in mammalian disease tissue in vivo not shown
  20. 2025 Medium

    A mitoNEET/DHODH axis was identified as a downstream effector of ferroptosis defense, extending mitoNEET's anti-ferroptotic role to a specific enzymatic partner.

    Evidence mitoNEET KO/overexpression in TBI mice, DHODH siRNA epistasis, NL-1 pharmacology, ferroptosis and cognitive readouts

    PMID:40189124

    Open questions at the time
    • Single-lab, single-study finding
    • Direct physical/biochemical link between mitoNEET and DHODH not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CISD1's distinct biochemical activities — cluster donation, VDAC1 gating, FMNH2-to-ubiquinone electron transfer, and putative cysteine transaminase activity — are integrated and prioritized in vivo, and which underlies its mitophagy and neurodegeneration roles, remains unresolved.
  • No unified model linking enzymatic vs cluster-donor functions to phenotypes
  • Cysteine transaminase activity (idx 41) awaits independent replication
  • Mammalian in vivo relevance of the pathogenic disulfide dimer untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0005198 structural molecule activity 1 GO:0098772 molecular function regulator activity 1
Localization
GO:0005739 mitochondrion 3
Pathway
R-HSA-5357801 Programmed Cell Death 3 R-HSA-9612973 Autophagy 3 R-HSA-1430728 Metabolism 2 R-HSA-382551 Transport of small molecules 2
Partners
ACO1CISD2DHODHFDX1GLUD1VDAC1

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 mitoNEET (CISD1) was identified as a novel mitochondrial binding target of pioglitazone by photoaffinity cross-linking; it is a <17-kDa protein located in the mitochondrial fraction and was found to associate with a complex of solubilized mitochondrial proteins including the trifunctional beta-oxidation protein. Photoaffinity cross-linking with tritiated pioglitazone, mass spectrometry, NH2-terminal sequencing, Western blot, size exclusion chromatography, solid-phase pulldown American journal of physiology. Endocrinology and metabolism High 14570702
2007 mitoNEET is an integral outer mitochondrial membrane protein with an N-terminal transmembrane anchor and a cytoplasm-facing CDGSH domain containing 1.6 mol Fe per mole protein; cardiac mitochondria from mitoNEET-null mice show reduced oxidative capacity, establishing its role in controlling maximal mitochondrial respiratory rates. Bioinformatic analysis, iron quantification, subcellular fractionation/localization, mitoNEET-null mouse model with mitochondrial respiration assays Proceedings of the National Academy of Sciences of the United States of America High 17376863
2007 X-ray crystal structure (1.5 Å) of mitoNEET revealed a unique dimeric 'NEET fold' in which each protomer coordinates a 2Fe-2S cluster; pioglitazone binding stabilizes the protein against 2Fe-2S cluster release. X-ray crystallography at 1.5 Å, ligand-stability assays with pioglitazone Proceedings of the National Academy of Sciences of the United States of America High 17766440
2007 The 2Fe-2S cluster of mitoNEET is redox-active and pH-labile; mass spectrometry confirmed loss of 2Fe and 2S upon cofactor extrusion; spectroscopy showed the cluster is coordinated by Cys-3 and His-1 residues, with protonation of the His ligand triggering cluster release, suggesting a role in Fe-S cluster shuttling and/or redox reactions. Optical spectroscopy, electron paramagnetic resonance (EPR), mass spectrometry, recombinant mutagenesis The Journal of biological chemistry High 17584744
2007 Crystal structure of human mitoNEET soluble domain (residues 32–108) at 1.8 Å revealed an intertwined homodimer with a [2Fe-2S] cluster coordinated by three cysteines and one histidine (novel CCCH-type motif), and UV-visible spectra indicated redox (oxidized/reduced) states. X-ray crystallography at 1.8 Å, UV-visible absorption spectroscopy Proceedings of the National Academy of Sciences of the United States of America High 17766439
2007 Crystal structure of the cytoplasmic mitoNEET domain at high resolution confirmed [2Fe-2S] cluster coordination by Cys-72, Cys-74, Cys-83, and His-87; homodimerization is mediated by hydrophobic interactions and hydrogen bonds; His-87 is solvent-exposed and proposed to mediate interaction with other proteins. X-ray crystallography, analytical ultracentrifugation (homodimer in solution and crystal) The Journal of biological chemistry High 17905743
2007 CISD1 (mitoNEET) mRNA is down-regulated in cystic fibrosis cells and restored upon ectopic CFTR expression; a CISD1-GFP chimera localizes to mitochondria, demonstrating CFTR-dependent regulation of this mitochondrial protein. RT-PCR in cell lines with/without CFTR, CFTR inhibitors (glibenclamide, CFTR(inh)-172), cAMP stimulation, live-cell fluorescence imaging of CISD1-GFP Biochemical and biophysical research communications Medium 18047834
2009 Thiazolidinedione drug binding shifts the midpoint potential of the mitoNEET [2Fe-2S] cluster by more than 100 mV (from ~0 to −100 mV at pH 7); His87Cys mutation abolishes TZD's ability to affect the redox potential, indicating His87 mediates communication between the drug binding site and the Fe-S center. Protein film voltammetry (PFV), site-directed mutagenesis (H87C) Biochemistry High 19791753
2009 Resonance Raman spectra of mitoNEET show pH-dependent changes in the Fe-His87 region (250–300 cm⁻¹) absent in the H87C mutant, demonstrating that the Fe-N(His87) interaction is modulated within physiological pH range and that this modulation is coupled to cluster lability. Resonance Raman spectroscopy, comparison with H87C mutant Biochemistry Medium 19388667
2010 NADPH binds to homodimeric mitoNEET (at residues K55 and H58) and destabilizes the [2Fe-2S] clusters, promoting their release at pH ≤ 7.0 by disrupting inter-subunit interactions with H87′ and R73′. NMR spectroscopy, isothermal titration calorimetry, UV-visible absorption, circular dichroism Biochemistry High 20932062
2010 EPR analysis of reduced mitoNEET confirmed valence-localized [2Fe-2S] cluster with Fe²⁺ at the His-bound iron; inter-cluster dipolar coupling is detectable and the histidine N-delta coordinates to iron with A_iso = −6.25 MHz. Multifrequency/multitechnique EPR (CW, ESEEM, ENDOR, HYSCORE), ¹⁵N-labeling Journal of the American Chemical Society High 20099820
2011 mitoNEET transfers its [2Fe-2S] cluster to apo-ferredoxin in a unidirectional, second-order reaction; His87 is required for cluster transfer (H87C mutant inhibits transfer), while the Lys55Glu mutation does not; pioglitazone inhibits iron transfer from mitoNEET to mitochondria in HEK293 cells. UV-VIS spectroscopy, native-PAGE, mitochondrial iron detection assay in cells, site-directed mutagenesis (H87C, K55E) Proceedings of the National Academy of Sciences of the United States of America High 21788481
2011 Crystal structure of H87C mitoNEET at 1.7 Å showed that replacing His87 with Cys stabilizes the cluster ~6-fold and decreases the redox potential ~300 mV; Cys87 displays two conformations; structural changes are localized to the cluster-binding region. X-ray crystallography at 1.7 Å, spectroscopic cluster stability assays Acta crystallographica. Section D, Biological crystallography High 21636891
2012 NADPH inhibits [2Fe-2S] cluster transfer from mitoNEET to an apo-acceptor protein (K_i = 200 µM); the conserved Asp-84 residue in the CDGSH domain is required for NADPH-dependent inhibition of cluster transfer. In vitro cluster transfer assay, site-directed mutagenesis (D84 variants), inhibition kinetics The Journal of biological chemistry High 22351774
2012 mitoNEET overexpression in adipocytes inhibits mitochondrial iron transport into the matrix, reducing electron transport chain activity, lowering β-oxidation rates, mitochondrial membrane potential, and ROS production; mitoNEET knockdown enhances mitochondrial respiratory capacity through increased matrix iron. Transgenic mouse overexpression, shRNA knockdown, mitochondrial iron measurements, metabolic/respiration assays Nature medicine High 22961109
2013 mitoNEET forms a covalent disulfide bond with glutamate dehydrogenase 1 (GDH1) and acts as an activator of GDH1; specific cysteine residues participating in the disulfide bond were identified by proteomics. Protein pulldown, SDS-PAGE, mass spectrometry/proteomics identification of disulfide bond Biochemistry Medium 24295216
2013 shRNA suppression of mitoNEET in breast cancer cells causes reduced cell proliferation, decreased mitochondrial performance, uncontrolled accumulation of mitochondrial iron and ROS, and activation of autophagy. shRNA knockdown, cell proliferation assays, mitochondrial iron/ROS imaging, autophagy assays, xenograft tumor model Proceedings of the National Academy of Sciences of the United States of America High 23959881
2013 TNFα-induced necroptosis in hepatocytes requires mitoNEET: fructose/ethanol overexpression of CISD1 primes cells for TNFα cytotoxicity; TNFα promotes translocation of a Stat3-Grim-19 complex to mitochondria, which binds mitoNEET and triggers rapid release of its 2Fe-2S cluster, causing mitochondrial iron accumulation, ROS surge, and cell death. Co-immunoprecipitation (Stat3-Grim-19 with mitoNEET), Western blot, mitochondrial iron measurement, L929 cell and hepatocyte necroptosis models Journal of cell science Medium 24357718
2014 mitoNEET Fe-S assembly strictly depends on mitochondrial ISC machinery (not CIA or CIAPIN1); augmenter of liver regeneration (ALR), a Mia40-dependent protein, is specifically required for mitoNEET maturation; holo-mitoNEET can repair oxidatively damaged Fe-S of IRP1/cytosolic aconitase, identifying IRP1 as a physiological acceptor of the mitoNEET Fe-S cluster. Genetic epistasis (siRNA depletion of ISC/CIA components), in vitro Fe-S assembly assay, cluster transfer to IRP1 after nitrosative stress, in vivo aconitase activity assay The Journal of biological chemistry High 25012650
2014 The [2Fe-2S] clusters of mitoNEET are reduced by glutathione/cysteine/DTT and can be reversibly oxidized by H₂O₂ without cluster disruption; human glutathione reductase efficiently reduces mitoNEET clusters via its redox-active disulfide, whereas rat thioredoxin reductase (selenocysteine-containing) has no such activity. In vitro biochemical reduction/oxidation assays, inhibitor (N-ethylmaleimide) studies, UV-visible spectroscopy The Journal of biological chemistry High 24403080
2015 Reduction of mitoNEET [2Fe-2S] clusters by human glutathione reductase proceeds via the enzyme's redox-active disulfide in an NADPH-dependent manner; N-ethylmaleimide abolishes this activity; rat thioredoxin reductase (selenocysteine) has negligible activity. In vitro enzyme assays, inhibitor studies, comparative enzyme analysis Free radical biology & medicine Medium 25645953
2015 MAD-28 (a cluvenone derivative) binds mitoNEET and breaks the coordinative bond between His87 and the cluster Fe, destabilizing the 2Fe-2S cluster; cancer cells with suppressed mitoNEET are less susceptible to MAD-28, confirming NEET proteins as direct drug targets. Docking analysis, cell-based functional assays, shRNA suppression epistasis, mitochondrial respiration and iron measurements Proceedings of the National Academy of Sciences of the United States of America Medium 25762074
2016 CISD1 (mitoNEET) negatively regulates ferroptosis in hepatocellular carcinoma cells by protecting against intramitochondrial lipid peroxidation; CISD1 expression is iron-dependently upregulated by erastin; genetic inhibition of CISD1 increases iron-mediated mitochondrial lipid peroxidation; pioglitazone-mediated stabilization of the Fe-S cluster inhibits mitochondrial iron uptake and lipid peroxidation. shRNA/siRNA knockdown, pioglitazone treatment, mitochondrial iron and lipid peroxidation measurements, erastin-induced ferroptosis model Biochemical and biophysical research communications High 27510639
2016 Only the oxidized [2Fe-2S]²⁺ state of mitoNEET is active in cluster transfer to acceptor proteins; the reduced [2Fe-2S]⁺ state is a dormant form resistant to cluster loss; dioxygen is not required for transfer and does not affect transfer rate; mitoNEET thus uses an iron-based redox switch to regulate cluster transfer. Controlled spectroscopic reduction/oxidation, anaerobic cluster transfer assays, UV-vis and EPR spectroscopy The Journal of biological chemistry High 26887944
2016 β-cell-specific overexpression of mitoNEET causes hyperglycemia via activation of a Parkin-dependent mitophagic pathway with vacuole and mitophagosome formation; α-cell-specific mitoNEET induction leads to hypoglycemia and protective effects on β-cells. Cell-type-specific transgenic mouse models, histology, electron microscopy of mitophagosomes, glucose tolerance tests Diabetes Medium 26895793
2016 Flavin mononucleotide (FMN) but not FAD has a specific interaction with mitoNEET (EPR evidence); reduced flavin nucleotides rapidly reduce mitoNEET [2Fe-2S] clusters as electron shuttles, with one FMN molecule reducing ~100 mitoNEET clusters in 4 min. EPR spectroscopy, UV-vis absorption, flavin reductase/NADH assay system, molecular docking Free radical biology & medicine Medium 27923678
2017 mitoNEET is a redox enzyme that catalyzes electron transfer from FMNH₂ to oxygen or ubiquinone via its [2Fe-2S] clusters; ubiquinone-2 is a more efficient oxidant than O₂; pioglitazone inhibits this electron transfer activity by forming a unique complex with mitoNEET and FMNH₂. In vitro reconstituted electron transfer assay (FMN/NADH/flavin reductase system), UV-vis spectroscopy, anaerobic and aerobic conditions The Journal of biological chemistry High 28461337
2017 mitoNEET KO cells show reduced frequency of intermitochondrial junctions and decreased total mitochondrial volume (reducing cellular respiration); mitoNEET overexpression strongly increases intermitochondrial contacts and causes mitochondrial clustering; a mitoNEET mutant resistant to oxidative stress increases H₂O₂ resistance of the mitochondrial network. 3D-EM reconstruction, thin-section EM, respiration assays in KO cells, re-expression rescue experiments Proceedings of the National Academy of Sciences of the United States of America High 28716905
2017 mitoNEET and NAF-1 (CISD2) directly interact in mammalian cells; mitoNEET can transfer its [2Fe-2S] clusters to NAF-1 in vitro; single and double shRNA knockdown establishes they function in the same cellular pathway controlling mitochondrial iron and ROS. Yeast two-hybrid, in vivo bimolecular fluorescence complementation (BiFC), direct coupling analysis, in vitro cluster transfer assay, shRNA knockdown with iron/ROS imaging PloS one High 28426722
2017 The cytosolic electron donor complex Ndor1/anamorsin (CIA machinery) reduces mitoNEET [2Fe-2S] clusters via transient protein-protein interaction, bringing their clusters into proximity; this provides a direct mechanistic link between CIA machinery and the mitoNEET cluster transfer/repair pathway. UV-vis and NMR spectroscopy in vitro, complex formation characterization Journal of the American Chemical Society Medium 28648056
2017 Loss of mitoNEET in striatum results in mitochondrial dysfunction (elevated ROS, reduced ATP production), loss of striatal dopamine and tyrosine hydroxylase, shortened gait, and reduced rotarod performance, consistent with a Parkinson's disease-like phenotype. CISD1 knockout mice, isolated mitochondria ROS and ATP assays, immunohistochemistry for TH/dopamine, gait analysis, rotarod ACS chemical neuroscience Medium 28880525
2018 pH regulates mitoNEET cluster transfer activity around physiological cytosolic pH; mitoNEET is highly resistant to H₂O₂ compared to other Fe-S cluster transfer proteins (ISCU, SufB); only one of two mitoNEET clusters is transferred when the other is decomposed; direct cluster transfer to apo-ferredoxin (not via intermediary) is confirmed. In vitro cluster transfer assays at varying pH, H₂O₂ resistance assays vs. ISCU/SufB, biophysical approaches (native MS, spectroscopy) Biochemistry High 30204426
2018 Electron transfer kinetics of mitoNEET: FMNH₂ rapidly reduces [2Fe-2S] clusters; O₂ oxidizes reduced clusters at ~6 M⁻¹s⁻¹; ubiquinone-2 oxidizes them at ~3×10³ M⁻¹s⁻¹, ~500-fold faster than O₂, supporting ubiquinone as the intrinsic electron acceptor in mitochondria. Stopped-flow kinetics, UV-vis spectroscopy under anaerobic and aerobic conditions Free radical biology & medicine High 29704621
2019 Oxidized mitoNEET gates VDAC1 in a redox-dependent manner; mitoNEET binds VDAC1 at the DIDS-sensitive site in vitro; the VDAC inhibitor DIDS prevents both mitoNEET–VDAC1 binding in vitro and mitoNEET-dependent mitochondrial iron accumulation in situ, indicating mitoNEET closes VDAC1 to regulate metabolite flow. In vitro binding assay, DIDS inhibitor studies in cells and in vitro, mitochondrial iron accumulation assay Proceedings of the National Academy of Sciences of the United States of America High 31527235
2019 AGBE (glycogen branching enzyme) binds specifically to holo-IRP1 (aconitase) and to mitoNEET; this interaction facilitates nuclear translocation of holo-IRP1, demonstrating mitoNEET as part of a complex regulating iron-dependent gene expression. Co-immunoprecipitation, genetic studies in Drosophila, nuclear fractionation Nature communications Medium 31784520
2019 Crystal structure of mitoNEET soluble domain bound to sulfonamide ligand furosemide was determined; structural basis of drug binding site on mitoNEET was elucidated for rational drug design. X-ray crystallography of mitoNEET–furosemide complex Communications chemistry High 32382661
2020 FMN (and lumiflavin) forms a specific covalent complex with mitoNEET under blue light exposure near the [2Fe-2S] cluster; lumichrome (FMN analog lacking ribityl and phosphate) cannot mediate cluster redox transition and acts as a competitive inhibitor, mapping the FMN binding site. EPR spectroscopy, UV-vis, blue-light cross-linking, FMN analog comparison Free radical biology & medicine Medium 32445867
2020 Pioglitazone-mediated neuroprotection after TBI requires mitoNEET: pioglitazone mitigates Ca²⁺-induced mitochondrial dysfunction and provides neuroprotection in WT mice but not in mitoNEET-null mice, establishing mitoNEET as the necessary mediator of pioglitazone's neuroprotective effects. WT and CISD1-null mouse TBI model, Ca²⁺-induced mitochondrial dysfunction assay, neuroprotection endpoints Experimental neurology High 32057797
2020 Single-molecule AFM force spectroscopy shows the Fe-N(His87) bond is the mechanically weakest point of the [2Fe-2S] cluster and its rupture can be independent of cluster break, enabling multiple unfolding pathways and a Fe₂S₂(Cys)₃ intermediate. AFM-based single-molecule force spectroscopy (AFM-SMFS) Analytical chemistry Medium 33048522
2021 Cardiac-specific deletion of CISD1 results in mitochondrial morphological abnormalities and elevated ROS at early time points, progressing to cardiac dysfunction at 12 months and heart failure by 16 months, demonstrating mitoNEET is required for maintaining cardiac mitochondrial integrity during aging. Cardiac-specific CISD1 KO mouse on C57BL/6J background, echocardiography, electron microscopy, ROS measurements Communications biology High 33514783
2021 Pioglitazone stabilizes the labile Fe(III)-N(His87) bond of the mitoNEET cluster ~10-fold (by AFM-SMFS), while reducing dissociation of other protein regions only ~3-fold; this Fe-N bond stabilization is the primary mechanism by which pioglitazone inhibits metal cluster transfer. AFM-based single-molecule force spectroscopy with a mitoNEET homodimer polyprotein construct The journal of physical chemistry letters Medium 33856229
2022 mitoNEET binds pyridoxal phosphate (PLP) specifically at Lys55 and catalyzes transamination of cysteine and 2-oxoglutarate to form 3-mercaptopyruvate and glutamate, demonstrating cysteine transaminase enzymatic activity. PLP binding assay (Lys55-specific), in vitro transamination assay with amino acid substrates ACS chemical biology Medium 36194135
2022 Pharmacological inhibition of mitoNEET (NL-1 or rosiglitazone) induces PINK1-Parkin-mediated mitophagy; mitoNEET inhibition promotes Pink1/Parkin accumulation, mitochondria-lysosome crosstalk, and PGC-1α expression. NL-1 pharmacological inhibition, shRNA knockdown, Western blot of mitophagy markers (Pink1, Parkin, LC3), lysosome imaging in RAW264.7 cells BMB reports Medium 35725011
2024 CISD1 accumulation in Pink1 and parkin mutant Drosophila forms aberrant disulfide-linked dimers incapable of coordinating the Fe-S cluster; elevated Cisd blocks mitophagy and impairs autophagy flux; genetic or pharmacological reduction of Cisd/CISD1 rescues locomotion, lifespan, dopamine levels, and mitochondrial ultrastructure in Pink1/parkin mutants, placing CISD1 downstream of PINK1 in the mitophagy pathway. Drosophila Pink1/parkin mutant genetics, human iPSC dopaminergic neurons, disulfide bond detection, mitophagy/autophagy flux assays, NL-1/rosiglitazone pharmacology, epistasis by genetic rescue Molecular neurodegeneration High 38273330
2024 In Pink1 mutant flies and PINK1-mutant patient dopaminergic neurons, CISD1 forms aberrant disulfide-linked homodimers unable to bind the Fe-S cluster; overexpression of cluster-binding-deficient CISD1 worsens Pink1-mutant phenotypes, while complete loss of Cisd rescues all Pink1-mutant phenotypes, indicating that iron-depleted CISD1 is the pathogenic species operating downstream of PINK1. Drosophila genetics, human patient-derived dopaminergic neurons, disulfide dimer characterization, gain/loss-of-function with Fe-S binding mutant, behavioral and lifespan assays eLife High 39159312
2025 mitoNEET inhibition (NL-1) ameliorates TBI-induced ferroptosis and cognitive dysfunction through activation of the mitoNEET/DHODH (dihydroorotate dehydrogenase) signaling axis; silencing DHODH blocks the anti-ferroptosis effects of NL-1, establishing DHODH as a downstream effector of mitoNEET in ferroptosis defense. mitoNEET KO and overexpression in TBI mouse models, DHODH siRNA epistasis, NL-1 pharmacology, ferroptosis markers, cognitive testing Experimental neurology Medium 40189124

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 CISD1 inhibits ferroptosis by protection against mitochondrial lipid peroxidation. Biochemical and biophysical research communications 400 27510639
2012 MitoNEET-driven alterations in adipocyte mitochondrial activity reveal a crucial adaptive process that preserves insulin sensitivity in obesity. Nature medicine 398 22961109
2003 Identification of a novel mitochondrial protein ("mitoNEET") cross-linked specifically by a thiazolidinedione photoprobe. American journal of physiology. Endocrinology and metabolism 279 14570702
2007 MitoNEET is an iron-containing outer mitochondrial membrane protein that regulates oxidative capacity. Proceedings of the National Academy of Sciences of the United States of America 249 17376863
2007 MitoNEET is a uniquely folded 2Fe 2S outer mitochondrial membrane protein stabilized by pioglitazone. Proceedings of the National Academy of Sciences of the United States of America 228 17766440
2013 NAF-1 and mitoNEET are central to human breast cancer proliferation by maintaining mitochondrial homeostasis and promoting tumor growth. Proceedings of the National Academy of Sciences of the United States of America 172 23959881
2007 The outer mitochondrial membrane protein mitoNEET contains a novel redox-active 2Fe-2S cluster. The Journal of biological chemistry 133 17584744
2019 Redox-dependent gating of VDAC by mitoNEET. Proceedings of the National Academy of Sciences of the United States of America 118 31527235
2011 Facile transfer of [2Fe-2S] clusters from the diabetes drug target mitoNEET to an apo-acceptor protein. Proceedings of the National Academy of Sciences of the United States of America 110 21788481
2007 Crystal structure of human mitoNEET reveals distinct groups of iron sulfur proteins. Proceedings of the National Academy of Sciences of the United States of America 98 17766439
2014 The diabetes drug target MitoNEET governs a novel trafficking pathway to rebuild an Fe-S cluster into cytosolic aconitase/iron regulatory protein 1. The Journal of biological chemistry 95 25012650
2014 mitoNEET as a novel drug target for mitochondrial dysfunction. Drug discovery today 88 24814435
2007 Crystallographic studies of human MitoNEET. The Journal of biological chemistry 76 17905743
2017 MitoNEET (CISD1) Knockout Mice Show Signs of Striatal Mitochondrial Dysfunction and a Parkinson's Disease Phenotype. ACS chemical neuroscience 67 28880525
2014 MitoNEET-mediated effects on browning of white adipose tissue. Nature communications 66 24865177
2015 The Fe-S cluster-containing NEET proteins mitoNEET and NAF-1 as chemotherapeutic targets in breast cancer. Proceedings of the National Academy of Sciences of the United States of America 65 25762074
2016 Redox Control of the Human Iron-Sulfur Repair Protein MitoNEET Activity via Its Iron-Sulfur Cluster. The Journal of biological chemistry 64 26887944
2016 MitoNEET-Parkin Effects in Pancreatic α- and β-Cells, Cellular Survival, and Intrainsular Cross Talk. Diabetes 61 26895793
2010 Binding of histidine in the (Cys)3(His)1-coordinated [2Fe-2S] cluster of human mitoNEET. Journal of the American Chemical Society 61 20099820
2009 Redox characterization of the FeS protein MitoNEET and impact of thiazolidinedione drug binding. Biochemistry 59 19791753
2014 Redox control of human mitochondrial outer membrane protein MitoNEET [2Fe-2S] clusters by biological thiols and hydrogen peroxide. The Journal of biological chemistry 57 24403080
2017 The mitochondrial outer membrane protein mitoNEET is a redox enzyme catalyzing electron transfer from FMNH2 to oxygen or ubiquinone. The Journal of biological chemistry 54 28461337
2017 MitoNEET-dependent formation of intermitochondrial junctions. Proceedings of the National Academy of Sciences of the United States of America 49 28716905
2010 Structure-based design of a thiazolidinedione which targets the mitochondrial protein mitoNEET. Bioorganic & medicinal chemistry letters 47 20064719
2020 Bioenergetic restoration and neuroprotection after therapeutic targeting of mitoNEET: New mechanism of pioglitazone following traumatic brain injury. Experimental neurology 40 32057797
2017 Interactions between mitoNEET and NAF-1 in cells. PloS one 40 28426722
2007 CISD1 codifies a mitochondrial protein upregulated by the CFTR channel. Biochemical and biophysical research communications 40 18047834
2009 Resonance Raman studies of the (His)(Cys)3 2Fe-2S cluster of MitoNEET: comparison to the (Cys)4 mutant and implications of the effects of pH on the labile metal center. Biochemistry 38 19388667
2024 Mitochondrial CISD1/Cisd accumulation blocks mitophagy and genetic or pharmacological inhibition rescues neurodegenerative phenotypes in Pink1/parkin models. Molecular neurodegeneration 37 38273330
2019 Glycogen branching enzyme controls cellular iron homeostasis via Iron Regulatory Protein 1 and mitoNEET. Nature communications 37 31784520
2016 MicroRNA-127 targeting of mitoNEET inhibits neurite outgrowth, induces cell apoptosis and contributes to physiological dysfunction after spinal cord transection. Scientific reports 37 27748416
2022 Inhibition of mitoNEET attenuates LPS-induced inflammation and oxidative stress. Cell death & disease 36 35136051
2019 Isoliquiritigenin Induces Mitochondrial Dysfunction and Apoptosis by Inhibiting mitoNEET in a Reactive Oxygen Species-Dependent Manner in A375 Human Melanoma Cells. Oxidative medicine and cellular longevity 36 30805086
2015 Reduction of mitochondrial protein mitoNEET [2Fe-2S] clusters by human glutathione reductase. Free radical biology & medicine 36 25645953
2013 Conserved hydrogen bonding networks of MitoNEET tune Fe-S cluster binding and structural stability. Biochemistry 36 23758282
2023 Mitochondrial miR-12294-5p regulated copper-induced mitochondrial oxidative stress and mitochondrial quality control imbalance by targeted inhibition of CISD1 in chicken livers. Journal of hazardous materials 35 37364438
2017 MitoNEET in Perivascular Adipose Tissue Blunts Atherosclerosis under Mild Cold Condition in Mice. Frontiers in physiology 33 29311966
2017 Anamorsin/Ndor1 Complex Reduces [2Fe-2S]-MitoNEET via a Transient Protein-Protein Interaction. Journal of the American Chemical Society 32 28648056
2016 CISD1 in association with obesity-associated dysfunctional adipogenesis in human visceral adipose tissue. Obesity (Silver Spring, Md.) 32 26692580
2009 Continuous-wave and pulsed EPR characterization of the [2Fe-2S](Cys)3(His)1 cluster in rat MitoNEET. Journal of the American Chemical Society 31 19736979
2023 Mitoglitazone ameliorates renal ischemia/reperfusion injury by inhibiting ferroptosis via targeting mitoNEET. Toxicology and applied pharmacology 30 36870574
2016 MitoNEET Deficiency Alleviates Experimental Alcoholic Steatohepatitis in Mice by Stimulating Endocrine Adiponectin-Fgf15 Axis. The Journal of biological chemistry 29 27573244
2012 NADPH inhibits [2Fe-2S] cluster protein transfer from diabetes drug target MitoNEET to an apo-acceptor protein. The Journal of biological chemistry 29 22351774
2010 Binding of reduced nicotinamide adenine dinucleotide phosphate destabilizes the iron−sulfur clusters of human mitoNEET. Biochemistry 29 20932062
2021 Cardiac-specific loss of mitoNEET expression is linked with age-related heart failure. Communications biology 27 33514783
2021 MiR-127-3p targeting CISD1 regulates autophagy in hypoxic-ischemic cortex. Cell death & disease 27 33723216
2018 MitoNEET in Perivascular Adipose Tissue Prevents Arterial Stiffness in Aging Mice. Cardiovascular drugs and therapy 27 30022354
2011 Novel ligands that target the mitochondrial membrane protein mitoNEET. Journal of molecular graphics & modelling 27 21531159
2016 MitoNEET Protects HL-1 Cardiomyocytes from Oxidative Stress Mediated Apoptosis in an In Vitro Model of Hypoxia and Reoxygenation. PloS one 26 27243905
2016 Identification of small molecules that bind to the mitochondrial protein mitoNEET. Bioorganic & medicinal chemistry letters 26 27687671
2014 A novel MitoNEET ligand, TT01001, improves diabetes and ameliorates mitochondrial function in db/db mice. The Journal of pharmacology and experimental therapeutics 26 25503385
2018 The H2O2-Resistant Fe-S Redox Switch MitoNEET Acts as a pH Sensor To Repair Stress-Damaged Fe-S Protein. Biochemistry 24 30204426
2017 Model of the MitoNEET [2Fe-2S] Cluster Shows Proton Coupled Electron Transfer. Journal of the American Chemical Society 23 28055193
2016 His-87 ligand in mitoNEET is crucial for the transfer of iron sulfur clusters from mitochondria to cytosolic aconitase. Biochemical and biophysical research communications 23 26778000
2011 Mutation of the His ligand in mitoNEET stabilizes the 2Fe-2S cluster despite conformational heterogeneity in the ligand environment. Acta crystallographica. Section D, Biological crystallography 23 21636891
2024 Metallothionein Alleviates Glutathione Depletion-Induced Oxidative Cardiomyopathy through CISD1-Dependent Regulation of Ferroptosis in Murine Hearts. The American journal of pathology 22 38417695
2016 Flavin nucleotides act as electron shuttles mediating reduction of the [2Fe-2S] clusters in mitochondrial outer membrane protein mitoNEET. Free radical biology & medicine 22 27923678
2011 Interdomain communication revealed in the diabetes drug target mitoNEET. Proceedings of the National Academy of Sciences of the United States of America 21 21402934
2009 The novel 2Fe-2S outer mitochondrial protein mitoNEET displays conformational flexibility in its N-terminal cytoplasmic tethering domain. Acta crystallographica. Section F, Structural biology and crystallization communications 21 19574633
2019 Crystal structure of the mitochondrial protein mitoNEET bound to a benze-sulfonide ligand. Communications chemistry 20 32382661
2015 Novel thiazolidinedione mitoNEET ligand-1 acutely improves cardiac stem cell survival under oxidative stress. Basic research in cardiology 20 25725808
2013 Identification of disulfide bond formation between MitoNEET and glutamate dehydrogenase 1. Biochemistry 20 24295216
2011 Complexes of the outer mitochondrial membrane protein mitoNEET with resveratrol-3-sulfate. Biochemistry 20 21591687
2020 Single-Molecule Force Spectroscopy Reveals that the Fe-N Bond Enables Multiple Rupture Pathways of the 2Fe2S Cluster in a MitoNEET Monomer. Analytical chemistry 19 33048522
2019 The MitoNEET Ligand NL-1 Mediates Antileukemic Activity in Drug-Resistant B-Cell Acute Lymphoblastic Leukemia. The Journal of pharmacology and experimental therapeutics 19 31010844
2013 Mitoneet mediates TNFα-induced necroptosis promoted by exposure to fructose and ethanol. Journal of cell science 19 24357718
2012 Strand swapping regulates the iron-sulfur cluster in the diabetes drug target mitoNEET. Proceedings of the National Academy of Sciences of the United States of America 19 22308404
2018 Electron transfer kinetics of the mitochondrial outer membrane protein mitoNEET. Free radical biology & medicine 18 29704621
2011 A novel binding assay identifies high affinity ligands to the rosiglitazone binding site of mitoNEET. Bioorganic & medicinal chemistry letters 18 21782425
2021 Pioglitazone Inhibits Metal Cluster Transfer of mitoNEET by Stabilizing the Labile Fe-N Bond Revealed at Single-Bond Level. The journal of physical chemistry letters 17 33856229
2021 Loss of the redox mitochondrial protein mitoNEET leads to mitochondrial dysfunction in B-cell acute lymphoblastic leukemia. Free radical biology & medicine 16 34496224
2023 MitoNEET prevents iron overload-induced insulin resistance in H9c2 cells through regulation of mitochondrial iron. Journal of cellular physiology 15 37269467
2022 Inhibition of mitoNEET induces Pink1-Parkin-mediated mitophagy. BMB reports 15 35725011
2021 The Mitochondrial mitoNEET Ligand NL-1 Is Protective in a Murine Model of Transient Cerebral Ischemic Stroke. Pharmaceutical research 15 33982226
2021 CISD1 protects against atherosclerosis by suppressing lipid accumulation and inflammation via mediating Drp1. Biochemical and biophysical research communications 15 34509082
2020 TT01001 attenuates oxidative stress and neuronal apoptosis by preventing mitoNEET-mediated mitochondrial dysfunction after subarachnoid hemorrhage in rats. Neuroreport 15 32604395
2024 Inhibition of CISD1 alleviates mitochondrial dysfunction and ferroptosis in mice with acute lung injury. International immunopharmacology 14 38377860
2022 Overexpression of CISD1 Predicts Worse Survival in Hepatocarcinoma Patients. BioMed research international 14 35313629
2020 Defects in CISD-1, a mitochondrial iron-sulfur protein, lower glucose level and ATP production in Caenorhabditis elegans. Biomedical journal 14 32200954
2020 Exploring the FMN binding site in the mitochondrial outer membrane protein mitoNEET. Free radical biology & medicine 13 32445867
2019 Quantitative Proteomics of Presynaptic Mitochondria Reveal an Overexpression and Biological Relevance of Neuronal MitoNEET in Postnatal Brain Development. Developmental neurobiology 13 31050203
2019 4-Hydroxynonenal and 4-Oxononenal Differentially Bind to the Redox Sensor MitoNEET. Chemical research in toxicology 12 31117349
2025 Inhibition of mitoNEET ameliorates traumatic brain injury-induced ferroptosis and cognitive dysfunction by stabilizing dihydroorotate dehydrogenase. Experimental neurology 11 40189124
2025 Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte. Journal of nanobiotechnology 11 40707955
2024 MitoNEET preserves muscle insulin sensitivity during iron overload by regulating mitochondrial iron, reactive oxygen species and fission. The FEBS journal 11 38944692
2022 The Intriguing mitoNEET: Functional and Spectroscopic Properties of a Unique [2Fe-2S] Cluster Coordination Geometry. Molecules (Basel, Switzerland) 11 36500311
2021 The long-standing relationship between paramagnetic NMR and iron-sulfur proteins: the mitoNEET example. An old method for new stories or the other way around? Magnetic resonance (Gottingen, Germany) 11 37904758
2012 Competition of zinc ion for the [2Fe-2S] cluster binding site in the diabetes drug target protein mitoNEET. Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine 11 22945239
2024 Inhibition of CISD1 attenuates cisplatin-induced hearing loss in mice via the PI3K and MAPK pathways. Biochemical pharmacology 10 38492782
2023 NL-1 Promotes PINK1-Parkin-Mediated Mitophagy Through MitoNEET Inhibition in Subarachnoid Hemorrhage. Neurochemical research 10 37828361
2021 New Insights of the NEET Protein CISD2 Reveals Distinct Features Compared to Its Close Mitochondrial Homolog mitoNEET. Biomedicines 10 33916457
2017 Combined Biochemical, Biophysical, and Cellular Methods to Study Fe-S Cluster Transfer and Cytosolic Aconitase Repair by MitoNEET. Methods in enzymology 10 28882209
2009 Chapter 13 Localization and function of the 2Fe-2S outer mitochondrial membrane protein mitoNEET. Methods in enzymology 10 19348892
2024 Iron-sulfur cluster loss in mitochondrial CISD1 mediates PINK1 loss-of-function phenotypes. eLife 9 39159312
2022 Novel mitoNEET ligand NL-1 improves therapeutic outcomes in an aged rat model of cerebral ischemia/reperfusion injury. Experimental neurology 9 35662609
2008 Crystallization and preliminary X-ray diffraction studies of the prototypal homologue of mitoNEET (Tth-NEET0026) from the extreme thermophile Thermus thermophilus HB8. Acta crystallographica. Section F, Structural biology and crystallization communications 9 19052371
2022 MitoNEET's Reactivity of Lys55 toward Pyridoxal Phosphate Demonstrates its Activity as a Transaminase Enzyme. ACS chemical biology 8 36194135
2021 NRVS and DFT of MitoNEET: Understanding the Special Vibrational Structure of a [2Fe-2S] Cluster with (Cys)3(His)1 Ligation. Biochemistry 8 34310123
2024 Loss of the mitochondrial protein mitoNEET in mice is associated with cognitive impairments and increased neuroinflammation. Journal of Alzheimer's disease : JAD 7 39639511
2022 Structure and biological evaluation of Caenorhabditis elegans CISD-1/mitoNEET, a KLP-17 tail domain homologue, supports attenuation of paraquat-induced oxidative stress through a p38 MAPK-mediated antioxidant defense response. Advances in redox research 7 36533211

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