Affinage

RHOT1

Mitochondrial Rho GTPase 1 · UniProt Q8IXI2

Length
618 aa
Mass
70.8 kDa
Annotated
2026-04-28
100 papers in source corpus 42 papers cited in narrative 42 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RHOT1 (Miro1) is an outer mitochondrial membrane GTPase that functions as a central adaptor coupling mitochondria to cytoskeletal motor systems and integrating Ca²⁺ signals to control organelle positioning, dynamics, and quality control across diverse cell types. Miro1 links mitochondria to kinesin (via TRAK1/2) and dynein motors for microtubule-based transport, with Ca²⁺ binding to its EF-hand domains arresting transport at sites of elevated cytosolic Ca²⁺ such as synapses; it also recruits myosin XIX for actin-based movement, promotes ER–mitochondria contact site formation through its N-terminal GTPase domain and interactions with VDAC1/IP3R, and negatively regulates Drp1-dependent fission at both mitochondria and peroxisomes (PMID:19249275, PMID:30111583, PMID:40176126, PMID:40214436, PMID:31894645). Miro1 is a direct Parkin ubiquitination substrate whose PINK1/Parkin/LRRK2-dependent removal from damaged mitochondria is a prerequisite for mitophagy—a step impaired in the majority of Parkinson's disease patient fibroblasts—and heterozygous RHOT1 mutations (R272Q, others) cause Ca²⁺ dyshomeostasis, α-synuclein accumulation, and dopaminergic neuron loss in human neurons and knock-in mice (PMID:24647965, PMID:31564441, PMID:39913247). Beyond neurons, splice variants containing an N-terminal insertion target Miro1 to peroxisomes via Pex19 to drive peroxisome motility and membrane elongation, and Miro1-dependent peripheral mitochondrial positioning generates local ATP:ADP and H₂O₂ gradients that sustain focal adhesion dynamics, cell migration, intercellular mitochondrial transfer through tunneling nanotubes, and cell-cycle progression (PMID:29222186, PMID:28615318, PMID:33341544, PMID:24431222, PMID:40214436).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2008 High

    Establishing how Miro1 connects mitochondria to microtubule motors: Miro1 was shown to recruit the kinesin adaptor TRAK2 (Grif-1) via its first GTPase domain, forming the core transport complex that drives anterograde mitochondrial movement in neurons.

    Evidence Co-immunoprecipitation with GTPase domain mutants and live mitochondrial trafficking assays in hippocampal neurons

    PMID:19103291

    Open questions at the time
    • Whether TRAK1 and TRAK2 are functionally redundant in this complex
    • Structural basis of the Miro1-TRAK interaction was unknown
  2. 2009 High

    Revealing the Ca²⁺-sensing mechanism that stops mitochondria: Ca²⁺ binding to Miro1 EF-hand domains at micromolar concentrations was found to disrupt the Miro1–kinesin linkage, providing a molecular switch by which neuronal activity halts mitochondrial transport at sites of demand.

    Evidence EF-hand mutagenesis combined with live imaging and glutamate/NMDA receptor stimulation in hippocampal neurons

    PMID:19249275

    Open questions at the time
    • Whether Ca²⁺ acts by direct conformational change in the EF-hands or via an intermediary
    • Role of the second EF-hand pair remained undefined
  3. 2013 High

    Linking psychiatric disease biology to the Miro1 transport complex: DISC1, a schizophrenia-associated protein, was found to form a complex with TRAK1 and Miro1 on mitochondria, and a disease variant impaired anterograde transport, broadening the pathological relevance of Miro1-mediated transport.

    Evidence Reciprocal co-immunoprecipitation, axonal mitochondrial tracking, and disease variant analysis in neurons

    PMID:24092329

    Open questions at the time
    • Whether DISC1 regulates Miro1 directly or through TRAK1
    • Structural basis of the DISC1–Miro1–TRAK1 tripartite interaction
  4. 2014 High

    Demonstrating Miro1 as a Parkin substrate central to mitophagy and establishing in vivo requirement for axonal transport: Parkin was shown to directly ubiquitinate Miro1 at defined lysines in a PINK1-dependent manner, and Miro1 knockout mice revealed depletion of axonal mitochondria causing upper motor neuron disease, separating transport and Ca²⁺-buffering functions.

    Evidence In vitro reconstituted ubiquitination with MS site-mapping; neuron-specific and global Miro1 KO mice with transport and neurological phenotyping

    PMID:24647965 PMID:25136135

    Open questions at the time
    • Whether Miro1 ubiquitination is sufficient or only necessary for mitophagy initiation
    • Relative contributions of individual ubiquitination sites
  5. 2014 High

    Extending Miro1 function to intercellular mitochondrial transfer and immune cell polarity: Miro1 was shown to drive mitochondrial transfer from mesenchymal stem cells to epithelial cells via tunneling nanotubes and to regulate dynein-dependent mitochondrial redistribution toward the MTOC during lymphocyte polarization and migration.

    Evidence Miro1 overexpression/knockdown in MSCs with in vivo airway injury models; co-IP with dynein and siRNA knockdown in lymphocytes under flow

    PMID:24431222 PMID:24492963

    Open questions at the time
    • Whether Miro1 directly engages the TNT formation machinery
    • Mechanism coupling integrin signaling to Miro1-dynein interaction
  6. 2015 High

    Revealing reciprocal feedback between Miro1-dependent mitochondrial positioning and local Ca²⁺/neurotransmitter release: Miro1 EF-hand-dependent synaptic positioning of mitochondria in astrocytes and presynaptic terminals was shown to homeostatically rescale Ca²⁺ signals and neurotransmitter release.

    Evidence EF-hand mutants with live imaging in hippocampal slices and genetically encoded presynaptic Ca²⁺ indicator (SyGCaMP5) with long-term activity manipulation

    PMID:26631479 PMID:28039205

    Open questions at the time
    • Whether Miro2 can compensate for Miro1 in this homeostatic mechanism
    • Molecular identity of Ca²⁺ buffering at presynaptic mitochondria
  7. 2017 High

    Connecting Miro1 to cell-autonomous bioenergetic control of migration and peroxisome biology: Miro1 loss caused perinuclear mitochondrial clustering, reduced peripheral ATP:ADP, and impaired focal adhesion/migration; independently, Miro1 splice variants containing an N-terminal insertion were found to target peroxisomes via Pex19, mediating long-range peroxisome motility.

    Evidence Miro1⁻/⁻ MEFs with ATP:ADP biosensor and migration assays; splice-variant identification with peroxisome localization and Pex19 receptor binding

    PMID:28615318 PMID:29222186

    Open questions at the time
    • How splice-variant ratio is regulated across tissues
    • Whether peroxisomal Miro1 also senses Ca²⁺
  8. 2018 High

    Identifying Miro1 as a dual-organelle motor adaptor and MCU interactor: Miro1 was established as the mitochondrial receptor for myosin XIX (actin-based transport) with GTPase-domain-regulated binding, and MCU was shown to directly interact with Miro1 through its outer membrane-spanning N-terminal domain, coupling mitochondrial Ca²⁺ uptake to transport.

    Evidence BioID proximity labeling with direct binding and GTPase mutants for Myo19; reciprocal co-IP with domain mapping for MCU; functional transport assays

    PMID:29694881 PMID:30111583

    Open questions at the time
    • Whether MCU–Miro1 interaction is modulated by mitochondrial Ca²⁺ load
    • Structural model of the Miro1–Myo19 interface
  9. 2019 High

    Establishing Miro1 removal as a universal biomarker of Parkinson's disease mitophagy failure and linking RHOT1 mutations to PD: Miro1 removal from depolarized mitochondria was impaired in >94% of PD patient fibroblasts across genetic backgrounds (PINK1, Parkin, LRRK2); separately, heterozygous RHOT1 coding mutations were found in PD patients to reduce ER–mitochondria contacts and cause Ca²⁺ dyshomeostasis.

    Evidence CCCP depolarization in large PD patient fibroblast cohort with genetic analysis; live-cell MERC imaging and Ca²⁺ measurement in RHOT1-mutant patient fibroblasts

    PMID:31303019 PMID:31564441

    Open questions at the time
    • Whether restoring Miro1 removal rescues mitophagy in all PD genetic backgrounds
    • RHOT1 variant penetrance and prevalence in large PD cohorts
  10. 2020 High

    Resolving Miro1's role at ER–mitochondria contacts and in ROS-dependent signaling: Miro1 was shown to interact with VDAC1, and its deletion restricted H₂O₂ distribution to perinuclear space, impairing peripheral redox signaling at focal adhesions; Miro1's GTPase domain was separately found to negatively regulate Drp1-dependent peroxisomal fission.

    Evidence Miro1⁻/⁻ MEFs with HyPer7 H₂O₂ biosensor and focal adhesion phospho-protein analysis; Miro1/2 KO cells with Drp1 fission assays; Co-IP of MIRO-1–VDAC-1 with point mutagenesis in C. elegans

    PMID:31894645 PMID:33341544 PMID:37306041

    Open questions at the time
    • Whether Miro1–VDAC1 interaction is direct in mammalian cells or requires bridging factors
    • Mechanism by which Miro1 inhibits Drp1 recruitment
  11. 2021 High

    Demonstrating Miro1 as a Ca²⁺-dependent negative regulator of mitofusin-mediated outer membrane fusion: Miro1 interacts with MFN and, through its EF-hand domains, inhibits MFN-mediated fusion when mitochondrial Ca²⁺ is elevated, positioning Miro1 as a central coordinator of mitochondrial dynamics beyond transport.

    Evidence Co-IP and proximity labeling proteomics, MCU inhibitor epistasis, EF-hand mutagenesis, and mitochondrial fusion assays

    PMID:34431132

    Open questions at the time
    • Whether Miro1 inhibits MFN by direct conformational restraint or sequestration
    • Whether this mechanism operates at peroxisomes as well
  12. 2022 High

    Defining dopaminergic neuron-specific consequences of Miro1 EF-hand mutations and Ser156 phosphoregulation: Miro1 R272Q knock-in iPSC dopaminergic neurons showed mitochondrial fragmentation, impaired respiration, and reduced dopamine uptake; separately, S156A knock-in depleted Miro1 and impaired OXPHOS complex III/V, linking PINK1-site phosphorylation to steady-state Miro1 levels.

    Evidence CRISPR isogenic knock-in iPSC-derived dopaminergic neurons with Ca²⁺ imaging, Seahorse respiration, dopamine uptake assays, and OXPHOS complex analysis

    PMID:35455950 PMID:36533136

    Open questions at the time
    • Whether S156 phosphorylation primes Miro1 for Parkin ubiquitination in vivo
    • Contribution of other PINK1 phosphosites on Miro1
  13. 2025 High

    Structural resolution of the Miro1–TRAK1 and Miro1–Parkin interfaces: Cryo-EM revealed two TRAK1-binding sites spanning the nGTPase, EF-hand pairs, and cGTPase of Miro1, with the complex forming a dimer; independently, a conserved Parkin linker region was identified as the substrate-interacting domain for Miro1, enabling Parkin recruitment prior to full activation.

    Evidence Cryo-EM structure with mutagenesis and cell-based localization assays; in vitro binding/ubiquitination reconstitution with domain mapping

    PMID:40576561 PMID:40615373

    Open questions at the time
    • Full-length Miro1–TRAK1–kinesin quaternary complex structure not yet resolved
    • Whether the Parkin substrate-interacting region also recognizes other OMM substrates
  14. 2025 High

    Linking Miro1 EF-hand dysfunction to α-synuclein pathology in vivo: R272Q (R285Q in mouse) knock-in caused calpain-mediated α-synuclein cleavage, phospho-α-synuclein accumulation in striatum, and dopaminergic neuron loss in substantia nigra, directly connecting Miro1 Ca²⁺ sensing to synucleinopathy.

    Evidence iPSC-derived midbrain organoids and CRISPR knock-in mice with calpain activity assays, α-synuclein immunohistochemistry, and behavioral tests

    PMID:39913247

    Open questions at the time
    • Whether calpain activation is a universal downstream effector of all Miro1 EF-hand mutations
    • Whether Miro1-directed therapies can reverse established α-synuclein pathology
  15. 2025 High

    Establishing Miro1 as a regulator of ER–mitochondria contacts during neuronal differentiation and cell-cycle progression: Miro1 N-terminal GTPase domain promotes ERMC formation that reduces Drp1-Ser616 phosphorylation; MIRO1 deficiency blocks G1/S progression and MERC formation, with MIRO1 interacting with VDAC1 and IP3R at contact sites.

    Evidence GTPase domain mutants in primary and iPSC neurons with AAV in vivo delivery; MIRO1⁻/⁻ fibroblasts/VSMCs with proximity ligation and split-GFP contact assays

    PMID:40176126 PMID:40214436

    Open questions at the time
    • Which ER-resident tethering complex Miro1 engages to form MERCs
    • How cell-cycle kinases regulate Miro1 to control MERC dynamics

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the full quaternary structure of the Miro1–TRAK–motor–cargo complex on membranes; how Miro1's GTPase cycle is regulated (no GAP or GEF identified); the mechanism by which Miro1 inhibits Drp1 recruitment; and whether targeting Miro1 can therapeutically rescue mitophagy defects in Parkinson's disease.
  • No GEF or GAP identified for either GTPase domain
  • No full membrane-associated structural model of the transport complex
  • Therapeutic potential of modulating Miro1 levels or activity in neurodegeneration untested in clinical settings

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 5 GO:0008092 cytoskeletal protein binding 5 GO:0060090 molecular adaptor activity 5 GO:0098772 molecular function regulator activity 3
Localization
GO:0005739 mitochondrion 8 GO:0005777 peroxisome 3 GO:0005886 plasma membrane 3
Pathway
R-HSA-1643685 Disease 5 R-HSA-1852241 Organelle biogenesis and maintenance 5 R-HSA-162582 Signal Transduction 4 R-HSA-9612973 Autophagy 3 R-HSA-1640170 Cell Cycle 2 R-HSA-5357801 Programmed Cell Death 2
Partners
KIF5BMCUMYO19PINK1PRKNTRAK1TRAK2VDAC1
Complex memberships
Miro1–Myo19 actin transport complexMiro1–TRAK1/2–kinesin transport complexMiro1–dynein motor complex

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Miro1 links mitochondria to KIF5 kinesin motor proteins, enabling microtubule-based mitochondrial movement; Ca2+ binding to Miro1 EF-hand domains at micromolar concentrations inhibits this linkage, causing mitochondrial stopping in response to glutamate/NMDA receptor activation in neurons. Live-cell imaging, EF-hand domain mutagenesis, glutamate/NMDA receptor stimulation in hippocampal neurons, mitochondrial motility assays Neuron High 19249275
2008 Miro1 recruits the kinesin adaptor Grif-1 (TRAK2) to mitochondria in a manner dependent on the first GTPase domain of Miro1; this complex mediates anterograde mitochondrial transport into neuronal processes. Co-immunoprecipitation, overexpression/dominant-negative GTPase domain mutants, live mitochondrial trafficking assays in hippocampal neurons Molecular and cellular neurosciences High 19103291
2014 Miro1 is a direct ubiquitination substrate of the E3 ligase Parkin; PINK1 phosphorylation of Parkin at Ser65 is required for efficient Parkin-mediated ubiquitylation of Miro1 at conserved lysines (K153, K230, K235, K330, K572) in vitro. In vitro E3 ligase ubiquitylation assay with full-length recombinant Parkin and Miro1, mass spectrometry identification of ubiquitination sites, active-site/disease-mutation analysis Open biology High 24647965
2014 Miro1 knockout in mice causes depletion of mitochondria from corticospinal tract axons and defective retrograde axonal mitochondrial transport, resulting in progressive upper motor neuron disease; Miro1 is not required for Ca2+-mediated inhibition of mitochondrial movement or mitochondrial Ca2+ buffering per se. Neuron-specific and global Miro1 knockout mouse models, retrograde axonal transport assays, neurological phenotype characterization Proceedings of the National Academy of Sciences of the United States of America High 25136135
2014 Miro1 regulates intercellular mitochondrial transfer from mesenchymal stem cells to epithelial cells through tunneling nanotubes; overexpression of Miro1 in MSCs enhances transfer and rescue efficacy, while knockdown reduces it. Miro1 overexpression/knockdown in MSCs, live mitochondrial tracking, mouse models of airway injury, in vitro co-culture assays The EMBO journal High 24431222
2015 Miro1 Ca2+-sensing EF-hand domains regulate activity-driven mitochondrial positioning and confinement near synapses in astrocytic processes; Miro1-mediated mitochondrial positioning in turn reciprocally regulates intracellular Ca2+ levels in astrocytic processes. Live-cell confocal imaging in rat organotypic hippocampal slices, EF-hand domain mutants, neuronal activity stimulation The Journal of neuroscience High 26631479
2015 PINK1/Parkin-dependent degradation of Miro1 is the mechanism by which ALS mutant SOD1 inhibits anterograde axonal mitochondrial transport; overexpression of Miro1 or ablation of PINK1 rescues the transport deficit in mutant SOD1-expressing neurons. Miro1 overexpression rescue experiments, PINK1 ablation, Parkin-dependent knockdown in cortical and motor neurons from SOD1 G93A mice Human molecular genetics High 28973175
2016 Miro1-dependent activity-driven repositioning of mitochondria to presynaptic terminals (dependent on Miro1 Ca2+-sensing function) allows neurons to homeostatically rescale presynaptic Ca2+ signals and neurotransmitter release during prolonged activity changes. Live-cell imaging with genetically encoded presynaptic Ca2+ indicator (SyGCaMP5), Miro1 loss-of-function, long-term activity manipulation EMBO reports High 28039205
2017 Miro1-mediated mitochondrial positioning at the cell periphery and ventral surface creates intracellular ATP:ADP gradients; loss of Miro1 causes perinuclear clustering of mitochondria, reduces peripheral ATP:ADP ratio, impairs actin dynamics, lamellipodia protrusion, focal adhesion assembly, and slows cell migration. Miro1-/- mouse embryonic fibroblasts, genetically encoded ATP:ADP biosensor, live-cell migration assays, focal adhesion imaging Molecular biology of the cell High 28615318
2014 Miro-1 associates with the dynein motor complex and regulates redistribution of mitochondria toward the MTOC in lymphocytes in response to integrin-dependent adhesion and CXCL12 chemokine signaling, supporting lymphocyte polarity and migration. Co-immunoprecipitation with dynein, Miro-1 siRNA silencing, live mitochondrial tracking in lymphocytes under physiological flow conditions Molecular and cellular biology High 24492963
2018 Miro1 EF-hand domain 1 mediates a cytosolic Ca2+-induced mitochondrial shape transition (MiST) distinct from canonical fission/swelling; Ca2+-dependent disruption of the Miro1/KIF5B/tubulin complex is determined by this EF1 domain, and Miro1-dependent MiST is required for autophagy/mitophagy. EF-hand domain mutagenesis, live-cell imaging, KIF5B co-immunoprecipitation, autophagy/mitophagy flux assays in multiple cell types Cell reports High 29694881
2018 Miro1 and Miro2 are direct mitochondrial receptors for myosin XIX (Myo19); Miro1 binds directly to the C-terminal tail of Myo19, and this interaction is regulated by the nucleotide state of Miro1's N-terminal Rho-like GTPase domain; Myo19 protein stability depends on its association with Miro1/2. Proximity labeling (BioID), direct binding assays, in vivo recruitment assays, GTPase-domain mutants, Miro1/2 knockdown Journal of cell science High 30111583
2019 Miro1 removal from the outer mitochondrial membrane upon mitochondrial depolarization is a prerequisite for mitophagy; this Miro1 removal step is impaired in >94% of Parkinson's disease patient fibroblasts; PINK1, Parkin, and LRRK2 are required for Miro1 removal from damaged mitochondria. Biochemical depolarization assays in patient-derived skin fibroblasts, Miro1 level measurement after CCCP treatment, genetic analysis of PINK1/Parkin/LRRK2 patients Cell metabolism High 31564441
2013 DISC1 forms a complex with TRAK1 and Miro1 on mitochondria and promotes anterograde mitochondrial transport in neuronal axons; a psychiatric disease-associated DISC1 variant (37W) impairs anterograde mitochondrial transport. Co-immunoprecipitation, axonal mitochondrial tracking in neurons, disease variant analysis Human molecular genetics High 24092329
2019 Heterozygous RHOT1 mutations (c.815G>A; c.1348C>T) in PD patients reduce mitochondrial mass, decrease ER-mitochondria contact sites (MERCs), and cause calcium dyshomeostasis and increased mitophagy in patient-derived fibroblasts. Live-cell imaging of MERCs and Ca2+ homeostasis, immunocytochemistry, patient-derived fibroblast models with RHOT1 mutations Antioxidants & redox signaling High 31303019
2018 Miro1 (and Miro2) localize to peroxisomes and function as adaptors for microtubule-dependent peroxisome motility; peroxisome-targeted Miro1 contributes pulling forces that promote peroxisome membrane elongation and proliferation. Live-cell imaging, mathematical modeling of peroxisome motility, peroxisome-targeted Miro1 fusion constructs, microscopy in cellular models of peroxisome disease Traffic High 29364559
2017 Splicing variants of Miro1 containing an N-terminal insertion (insertion 1, recognized by cytosolic peroxisomal receptor Pex19) localize to peroxisomes and promote long-range microtubule-dependent peroxisomal movement via TRAK2. Identification of splice variants, peroxisome localization imaging, Miro1 knockdown and re-expression, Pex19 receptor interaction The Journal of cell biology High 29222186
2020 Peroxisomal localization of Miro1/2 (mediated by interaction of Miro transmembrane domain with Pex19 and regulated by Miro's first GTPase domain) is required for negative regulation of Drp1-dependent peroxisomal fission and maintenance of peroxisome size and morphology. Miro1/2 knockout cells, Drp1 fission assays, Pex19 interaction studies, GTPase domain mutants, live-cell imaging EMBO reports High 31894645
2020 MCU (mitochondrial calcium uniporter) interacts directly with Miro1 through MCU's N-terminal transmembrane domain that traverses the outer mitochondrial membrane; this interaction is required for Miro1-directed mitochondrial movement, identifying Miro1 as a component of the MCU complex. Co-immunoprecipitation, domain deletion/truncation mapping, mitochondrial localization assays, mitochondrial movement assays in neurons The Journal of neuroscience High 29686046
2020 Crystal structure of human Miro1 N-terminal GTPase domain bound to GTP at 1.7 Å reveals a non-catalytic active site configuration; SAXS data reveal a crescent-shaped assembly of the full soluble Miro1/2 domains; two conserved surfaces (SELFYY and ITIP motifs) are identified as potential dimerization or partner-binding interfaces. X-ray crystallography (1.7 Å), small angle X-ray scattering (SAXS), structural modeling Journal of structural biology High 33132189
2020 Miro1-mediated mitochondrial positioning controls subcellular H2O2 distribution; deletion of Miro1 restricts H2O2 to perinuclear space and reduces peripheral H2O2, impairing cytosolic PRX2 oxidation, focal adhesion signaling (vinculin/p130Cas phosphorylation), and focal adhesion size. Miro1-/- MEFs, HyPer7 genetically encoded H2O2 biosensor, rotenone treatment, focal adhesion imaging and phospho-protein analysis Redox biology High 33341544
2021 Miro1 functions as an inhibitory regulator of Mitofusin (MFN)-mediated outer mitochondrial membrane fusion in response to elevated mitochondrial Ca2+ ([Ca2+]m); Miro1 interacts with MFN as shown by Co-IP and proximity labeling proteomics; Miro1 EF-hand mutation compromises this Ca2+-dependent inhibitory effect. Co-immunoprecipitation, proximity labeling proteomics, MCU inhibitor and Miro1/2 knockdown, EF-hand mutagenesis, mitochondrial fusion assays Journal of cellular biochemistry High 34431132
2022 Miro1 R272Q (located in the Ca2+-binding EF-hand domain) in heterozygous knock-in human dopaminergic neurons causes mitochondrial fragmentation with reduced cristae and ATP5A, dampened mitochondrial Ca2+ buffering, reduced mitochondrial respiration, and impaired catecholamine (dopamine) neurotransmitter uptake; these synaptic changes are linked to Ca2+ handling at the outer mitochondrial membrane via monoamine oxidase. CRISPR knock-in iPSC-derived dopaminergic neurons, MCU inhibition phenocopy, Ca2+ imaging, mitochondrial respiration assays, dopamine uptake assays Frontiers in molecular neuroscience High 36533136
2022 The mDia2 formin stabilizes MIRO1 protein in cancer-associated fibroblasts; loss of mDia2 or MIRO1 reduces mitochondrial presence and ATP near the plasma membrane and CAF-tumor contact sites, causing metabolic dysfunction and suppressing protumorigenic protein secretion. mDia2/MIRO1 loss-of-function in fibroblasts and CAFs, ATP imaging at plasma membrane, metabolic assays, mouse squamous carcinogenesis models Cancer research High 35997559
2025 Cryo-EM structure of TRAK1569-623 bound to Miro1 reveals two binding sites: TRAK1569-623 binds in a cleft between Miro1's nGTPase and first EF-hand pair; TRAK1425-428 binds in a pocket between the second EF-hand pair and cGTPase; the complex forms a dimer mediated through the second EF-hand pair and cGTPase; both sites contribute to TRAK1 mitochondrial localization as validated by mutagenesis. Cryo-electron microscopy structure determination, mutagenesis, binding assays, cell-based mitochondrial localization assays Nature communications High 40615373
2025 A conserved region in the flexible linker between the Ubl and RING0 domains of Parkin (substrate-interacting region) directly interacts with Miro1 and is required for Parkin-mediated Miro1 ubiquitination; this provides a biochemical basis for Miro1-dependent Parkin recruitment to the mitochondrial membrane prior to full Parkin activation. In vitro binding and ubiquitination reconstitution, domain mapping/mutagenesis, cell-based Parkin recruitment assays The Journal of cell biology High 40576561
2025 Miro1 p.R272Q knock-in iPSC-derived dopaminergic neurons and midbrain organoids show increased oxidative stress, disrupted mitochondrial bioenergetics, elevated α-synuclein, and significant dopaminergic neuron loss; the R272Q mutation (in the Ca2+-binding domain) disrupts Ca2+ homeostasis, activating calpain proteases that cleave α-synuclein. Knock-in mice (p.R285Q, mouse orthologue) accumulate phosphorylated α-synuclein in the striatum and lose dopaminergic neurons in substantia nigra. iPSC-derived neurons and midbrain organoids, isogenic controls, CRISPR knock-in mice, Ca2+ imaging, calpain activity assays, α-synuclein measurement, behavioral tests Brain : a journal of neurology High 39913247
2022 Phosphorylation of Miro1 at Ser156 (a putative PINK1 site) regulates Miro1 steady-state protein levels and OXPHOS complex III and V abundance in mature dopaminergic neurons; S156A homozygous knock-in causes Miro1 depletion and impaired further degradation upon CCCP-induced mitophagy, and reduces mitochondrial oxygen consumption. CRISPR knock-in S156A iPSC-derived dopaminergic neurons, CCCP-induced mitophagy assays, mitochondrial respiration (Seahorse), OXPHOS complex analysis Cells High 35455950
2025 Miro1 N-terminal GTPase domain promotes ER-mitochondria contact (ERMC) formation in differentiating neurons; ERMC formation mediated by Miro1 decreases Drp1 phosphorylation at Ser616, reducing mitochondrial fission; glucocorticoid/prenatal stress selectively downregulates Miro1 and increases Drp1-Ser616 phosphorylation causing mitochondrial fragmentation and motility arrest. Primary hippocampal neurons and hiPSC-derived neurons, GTPase domain mutants (Miro1P26V), AAV-mediated overexpression in vivo, Ca2+ imaging at ERMCs, Drp1 phosphorylation assays Cell communication and signaling High 40176126
2025 MIRO1 controls an increase in the number of ER-mitochondria contact sites (MERCs) during G1/S cell cycle progression; MIRO1 deficiency blocks G1/S progression and cell-cycle-dependent MERCS formation; MIRO1 EF-hand domains and transmembrane domain are required for cell proliferation and MERC formation; MIRO1 interacts with VDAC1 and IP3R at MERCs (proximity-ligation assay). MIRO1-/- fibroblasts and VSMCs, proximity ligation assay (VDAC1/IP3R/GRP75/MIRO1), split-GFP ER/mitochondria contact assay, Ca2+ and ATP measurements, EF-hand and TM domain mutants Cells High 40214436
2023 MIRO-1 interacts directly with VDAC-1 at the outer mitochondrial membrane (interaction requiring MIRO-1 E473 and VDAC-1 K163) and this interaction is required for maintaining mitochondrial membrane potential in C. elegans; MIRO-1 E473G point mutation disrupts the interaction and reduces membrane potential. Co-immunoprecipitation, point mutagenesis (E473G in MIRO-1; K163 in VDAC-1), membrane potential measurement in C. elegans EMBO reports High 37306041
2020 Miro1-mutant (R272Q) patient-derived neurons show increased ER-mitochondria tethering (vs. fibroblasts which show decreased MERCs), impaired mitophagy flux, altered mitochondrial dynamics, and increased sensitivity to Ca2+ stress. Patient fibroblast-derived neurons, live-cell imaging of MERCs and mitochondrial dynamics, autophagy flux western blot, Ca2+ stress assays Human molecular genetics High 32280985
2016 Miro1 regulates mitochondrial motility and distribution in C. elegans; miro-1 mutation reduces mitochondrial amount by ~50% and extends lifespan in a daf-16/FOXO-dependent manner requiring loss of miro-1 from multiple tissues. C. elegans miro-1 loss-of-function genetics, lifespan assays, mitochondrial quantification, tissue-specific rescue experiments PloS one Medium 27064409
2016 In Xenopus embryos, Miro1 (Rhot1) is required for mitochondrial trafficking that drives aggregation of germinal granule components during primordial germ cell formation; expression of dominant-negative Rhot1ΔC (lacking the C-terminal transmembrane domain) inhibits germline-Mt aggregation and reduces PGC number. Dominant-negative Rhot1ΔC expression in Xenopus embryos, GFP-labeled mitochondria tracking, PGC counting at tail-bud stage Development, growth & differentiation Medium 27585825
2021 Miro1-directed mitochondrial trafficking in parvalbumin-positive (PV+) GABAergic interneurons is required for proper mitochondrial distribution and axonal arborization; loss of Miro1 in PV+ interneurons increases hippocampal γ-oscillation frequency and promotes anxiolysis. PV+ interneuron-specific Miro1 conditional KO mice, live and fixed imaging of mitochondrial distribution, ex vivo γ-oscillation electrophysiology, behavioral tests eLife High 34190042
2020 DISC1 regulates mitochondrial trafficking via the Miro1 GTPase domain; the first GTPase domain of Miro1 determines the direction of mitochondrial transport; a psychiatric disease-associated DISC1 mutation impairs Miro1's ability to transport mitochondria to synapses. GTPase-domain mutants of Miro1, DISC1 mutation analysis, mitochondrial trafficking direction assays in neurons, synaptic localization imaging Frontiers in cell and developmental biology Medium 32637409
2025 Miro1 knockout in mesenchymal stromal cells impairs mitochondrial association with microtubules and reduces mitochondrial transfer via tunneling nanotubes to ρ0 cancer cells in vivo, delaying tumor formation and mitochondrial respiration recovery. Inducible Miro1 KO mouse model, fluorescently labeled mitochondria tracking in vivo, TNT in vitro transfer assays, tumor growth measurements Cell reports High 39792553
2020 DAP3 triggers intrinsic apoptosis by promoting mitochondrial Ca2+ accumulation through the MCU complex, reducing cytosolic Ca2+; this reduction is sensed by Miro1, which subsequently drives mitochondrial fragmentation independently of canonical fission/fusion machinery. MCU depletion, Miro1 depletion, Ca2+ imaging, mitochondrial fragmentation and membrane potential assays, cell death assays MedComm Medium 40351389
2022 MIRO1 depletion in mouse oocytes disrupts mitochondrial distribution (causing perinuclear and cortical mitochondrial aggregates) and impairs polar body extrusion (~20% reduction), demonstrating MIRO1 as a mitochondrial adaptor setting mitochondrial distribution during oocyte maturation. Oocyte-specific MIRO1 conditional KO mice, live-cell mitochondrial tracking, polar body extrusion quantification, in vitro embryo development Frontiers in cell and developmental biology High 36325364
2023 miR-27-3p (highly expressed in lipotoxicity-polarized M1 macrophage exosomes) inactivates Miro1 through the miR-27-3p-Miro1 axis, causing mitochondrial fission over fusion, mitophagy impairment, NLRP3 activation, and insulin resistance; Miro1 inactivation by miR-27-3p drives type 2 diabetes development in high-fat-diet mice. miRNA mimic/inhibitor/antagomir in vitro and in vivo, siRNA-Miro1, exosome isolation and characterization, GTT and ITT, NLRP3 activation assays Diabetologia High 37615690
2025 MIRO1 regulates VSMC proliferation by: (1) maintaining mitochondrial cristae integrity and ETC complex I activity/supercomplex formation to support ATP synthesis, and (2) enabling Ca2+-dependent mitochondrial positioning via EF-hand domains to support cell-cycle G1/S progression; muscle-specific Miro1 deletion improves insulin action and oxidative capacity. Smooth muscle-specific Miro1 KO mice, carotid ligation neointima model, mitochondrial cristae imaging (TEM), ETC complex activity assays, EF-hand mutants, human coronary artery VSMC knockdown bioRxivpreprint Medium 39185180
2025 Accumulation of Miro1 in skeletal muscle of obese/T2D mice and humans is driven by impaired insulin-mediated AKT-Miro1 interaction at the outer mitochondrial membrane; muscle-specific Miro1 deletion improves insulin sensitivity and mitochondrial oxidative capacity; exercise training reduces skeletal muscle Miro1 accumulation and improves insulin sensitivity in T2D patients. Muscle-specific Miro1 KO mice, AKT-Miro1 interaction assays, randomized exercise intervention in T2D patients (N=24), mitochondrial respiration measurements medRxivpreprint Medium 41030931

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Miro1 is a calcium sensor for glutamate receptor-dependent localization of mitochondria at synapses. Neuron 543 19249275
2014 Miro1 regulates intercellular mitochondrial transport & enhances mesenchymal stem cell rescue efficacy. The EMBO journal 480 24431222
2016 iPSC-MSCs with High Intrinsic MIRO1 and Sensitivity to TNF-α Yield Efficacious Mitochondrial Transfer to Rescue Anthracycline-Induced Cardiomyopathy. Stem cell reports 210 27641650
2014 Loss of Miro1-directed mitochondrial movement results in a novel murine model for neuron disease. Proceedings of the National Academy of Sciences of the United States of America 185 25136135
2018 Miro1 Enhances Mitochondria Transfer from Multipotent Mesenchymal Stem Cells (MMSC) to Neural Cells and Improves the Efficacy of Cell Recovery. Molecules (Basel, Switzerland) 169 29562677
2017 Miro1-mediated mitochondrial positioning shapes intracellular energy gradients required for cell migration. Molecular biology of the cell 139 28615318
2008 GTPase dependent recruitment of Grif-1 by Miro1 regulates mitochondrial trafficking in hippocampal neurons. Molecular and cellular neurosciences 138 19103291
2019 Miro1 Marks Parkinson's Disease Subset and Miro1 Reducer Rescues Neuron Loss in Parkinson's Models. Cell metabolism 128 31564441
2014 Phosphorylation of Parkin at Serine65 is essential for activation: elaboration of a Miro1 substrate-based assay of Parkin E3 ligase activity. Open biology 115 24647965
2021 Circular RNA RHOT1 promotes progression and inhibits ferroptosis via mir-106a-5p/STAT3 axis in breast cancer. Aging 111 33686957
2015 Miro1 Regulates Activity-Driven Positioning of Mitochondria within Astrocytic Processes Apposed to Synapses to Regulate Intracellular Calcium Signaling. The Journal of neuroscience : the official journal of the Society for Neuroscience 109 26631479
2016 Miro1-dependent mitochondrial positioning drives the rescaling of presynaptic Ca2+ signals during homeostatic plasticity. EMBO reports 107 28039205
2014 Miro-1 links mitochondria and microtubule Dynein motors to control lymphocyte migration and polarity. Molecular and cellular biology 104 24492963
2020 Mitochondrial transfer from mesenchymal stem cells improves neuronal metabolism after oxidant injury in vitro: The role of Miro1. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 98 32501156
2018 MIRO-1 Determines Mitochondrial Shape Transition upon GPCR Activation and Ca2+ Stress. Cell reports 95 29694881
2018 Identification of Miro1 and Miro2 as mitochondrial receptors for myosin XIX. Journal of cell science 86 30111583
2017 Amyotrophic lateral sclerosis-associated mutant SOD1 inhibits anterograde axonal transport of mitochondria by reducing Miro1 levels. Human molecular genetics 85 28973175
2013 DISC1 complexes with TRAK1 and Miro1 to modulate anterograde axonal mitochondrial trafficking. Human molecular genetics 85 24092329
2023 Lipotoxicity-polarised macrophage-derived exosomes regulate mitochondrial fitness through Miro1-mediated mitophagy inhibition and contribute to type 2 diabetes development in mice. Diabetologia 76 37615690
2019 Mutations in RHOT1 Disrupt Endoplasmic Reticulum-Mitochondria Contact Sites Interfering with Calcium Homeostasis and Mitochondrial Dynamics in Parkinson's Disease. Antioxidants & redox signaling 70 31303019
2018 A role for Mitochondrial Rho GTPase 1 (MIRO1) in motility and membrane dynamics of peroxisomes. Traffic (Copenhagen, Denmark) 65 29364559
2008 EMB2473/MIRO1, an Arabidopsis Miro GTPase, is required for embryogenesis and influences mitochondrial morphology in pollen. The Plant cell 61 18344283
2015 Miro1 deficiency in amyotrophic lateral sclerosis. Frontiers in aging neuroscience 57 26074815
2018 MCU Interacts with Miro1 to Modulate Mitochondrial Functions in Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 50 29686046
2019 Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson's Disease Patients. Journal of clinical medicine 49 31888276
2019 Mitochondrial dysfunction is associated with Miro1 reduction in lung epithelial cells by cigarette smoke. Toxicology letters 48 31593750
2014 Miro1: new wheels for transferring mitochondria. The EMBO journal 47 24711517
2020 Impaired mitochondrial-endoplasmic reticulum interaction and mitophagy in Miro1-mutant neurons in Parkinson's disease. Human molecular genetics 46 32280985
2020 The Emerging Role of RHOT1/Miro1 in the Pathogenesis of Parkinson's Disease. Frontiers in neurology 45 33041957
2017 Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes. Oncotarget 45 29207597
2017 New splicing variants of mitochondrial Rho GTPase-1 (Miro1) transport peroxisomes. The Journal of cell biology 45 29222186
2020 Peroxisomal fission is modulated by the mitochondrial Rho-GTPases, Miro1 and Miro2. EMBO reports 39 31894645
2020 Miro1-mediated mitochondrial positioning supports subcellular redox status. Redox biology 35 33341544
2020 Miro1 Regulates Neuronal Mitochondrial Transport and Distribution to Alleviate Neuronal Damage in Secondary Brain Injury After Intracerebral Hemorrhage in Rats. Cellular and molecular neurobiology 31 32500352
2024 HMGB1 promotes mitochondrial transfer between hepatocellular carcinoma cells through RHOT1 and RAC1 under hypoxia. Cell death & disease 27 38378644
2021 Miro1-dependent mitochondrial dynamics in parvalbumin interneurons. eLife 27 34190042
2015 Miro1-mediated mitochondrial dysfunction under high nutrient stress is linked to NOD-like receptor 3 (NLRP3)-dependent inflammatory responses in rat pancreatic beta cells. Free radical biology & medicine 27 26427885
2023 Exosomal circRNA RHOT1 promotes breast cancer progression by targeting miR-204-5p/ PRMT5 axis. Cancer cell international 26 37924099
2022 Circular RNA RHOT1 Regulates miR-142-5p/CCND1 to Participate in Chondrocyte Autophagy and Proliferation in Osteoarthritis. Journal of immunology research 25 35300071
2015 Role of RHOT1 on migration and proliferation of pancreatic cancer. American journal of cancer research 25 26101710
2020 DISC1 Regulates Mitochondrial Trafficking in a Miro1-GTP-Dependent Manner. Frontiers in cell and developmental biology 23 32637409
2010 MIRO1 influences the morphology and intracellular distribution of mitochondria during embryonic cell division in Arabidopsis. Plant cell reports 23 20931334
2020 Insight into human Miro1/2 domain organization based on the structure of its N-terminal GTPase. Journal of structural biology 21 33132189
2020 Amyloid-beta oligomers induce Parkin-mediated mitophagy by reducing Miro1. The Biochemical journal 21 33155636
2022 A Protumorigenic mDia2-MIRO1 Axis Controls Mitochondrial Positioning and Function in Cancer-Associated Fibroblasts. Cancer research 20 35997559
2011 Arabidopsis thaliana MIRO1 and MIRO2 GTPases are unequally redundant in pollen tube growth and fusion of polar nuclei during female gametogenesis. PloS one 18 21494602
2021 Miro1 functions as an inhibitory regulator of MFN at elevated mitochondrial Ca2+ levels. Journal of cellular biochemistry 17 34431132
2016 C. elegans miro-1 Mutation Reduces the Amount of Mitochondria and Extends Life Span. PloS one 17 27064409
2022 Hsa_circ_0005230 is up-regulated and promotes gastric cancer cell invasion and migration via regulating the miR-1299/RHOT1 axis. Bioengineered 16 35170374
2025 The adaptor protein Miro1 modulates horizontal transfer of mitochondria in mouse melanoma models. Cell reports 14 39792553
2022 Miro1 R272Q disrupts mitochondrial calcium handling and neurotransmitter uptake in dopaminergic neurons. Frontiers in molecular neuroscience 14 36533136
2023 MIRO-1 interacts with VDAC-1 to regulate mitochondrial membrane potential in Caenorhabditis elegans. EMBO reports 13 37306041
2021 Propofol suppresses non-small cell lung cancer tumorigenesis by regulation of circ-RHOT1/miR-326/FOXM1 axis. Life sciences 13 33515563
2021 Miro1 Impairment in a Parkinson's At-Risk Cohort. Frontiers in molecular neuroscience 13 34434090
2022 Miro1 depletion disrupts spatial distribution of mitochondria and leads to oocyte maturation defects. Frontiers in cell and developmental biology 12 36325364
2020 Precision Neurology for Parkinson's Disease: Coupling Miro1-Based Diagnosis With Drug Discovery. Movement disorders : official journal of the Movement Disorder Society 12 32710675
2018 Lipopolysaccharide Mediates the Destruction of Intercellular Tight Junction among Renal Tubular Epithelial Cells via RhoT1/SMAD-4/JAM-3 Pathway. International journal of medical sciences 12 29725250
2023 Expression status of circ-SMARCA5, circ-NOL10, circ-LDLRAD3, and circ-RHOT1 in patients with colorectal cancer. Scientific reports 10 37587156
2021 Miro1 provides neuroprotection via the mitochondrial trafficking pathway in a rat model of traumatic brain injury. Brain research 10 34637761
2012 Genetic Screening of the Mitochondrial Rho GTPases MIRO1 and MIRO2 in Parkinson's Disease. The open neurology journal 10 22496713
2025 Parkinson's disease mutant Miro1 causes mitochondrial dysfunction and dopaminergic neuron loss. Brain : a journal of neurology 9 39913247
2020 Miro1 as a novel regulator of hypertrophy in neonatal rat cardiomyocytes. Journal of molecular and cellular cardiology 9 32234389
2019 HDAC6 and Miro1: Another interaction causing trouble in neurons. The Journal of cell biology 9 31118238
2025 Insufficient MIRO1 contributes to declined oocyte quality during reproductive aging. Science China. Life sciences 7 39815032
2022 Steady-State Levels of Miro1 Linked to Phosphorylation at Serine 156 and Mitochondrial Respiration in Dopaminergic Neurons. Cells 7 35455950
2022 Miro1 regulates mitochondrial homeostasis and meiotic resumption of mouse oocyte. Journal of cellular physiology 7 36183380
2020 The role of RHOT1 and RHOT2 genetic variation on Parkinson disease risk and onset. Neurobiology of aging 7 32948353
2025 Structural-functional characterization of the MIRO1-TRAK1 complex. Nature communications 6 40615373
2022 Interlinked role of ASN, TDP-43 and Miro1 with parkinopathy: Focus on targeted approach against neuropathy in parkinsonism. Ageing research reviews 6 36371014
2024 Armcx1 Reduces Neurological Damage Via a Mitochondrial Transport Pathway Involving Miro1 After Traumatic Brain Injury. Neuroscience 5 38492796
2024 A substrate-interacting region of Parkin directs ubiquitination of the mitochondrial GTPase Miro1. bioRxiv : the preprint server for biology 5 38895334
2021 Generation of R272Q, S156A and K572R RHOT1/Miro1 point mutations in iPSCs from a healthy individual using FACS-assisted CRISPR/Cas9 genome editing. Stem cell research 5 34359002
2018 Miro1 - the missing link to peroxisome motility. Communicative & integrative biology 5 30534345
2016 Mitochondrial trafficking through Rhot1 is involved in the aggregation of germinal granule components during primordial germ cell formation in Xenopus embryos. Development, growth & differentiation 5 27585825
2025 Miro1: A potential target for treating neurological disorders. Neuroscience 4 40403957
2024 Miro1 improves the exogenous engraftment efficiency and therapeutic potential of mitochondria transfer using Wharton's jelly mesenchymal stem cells. Mitochondrion 4 38408618
2023 Generation of two induced pluripotent stem cell lines and the corresponding isogenic controls from Parkinson's disease patients carrying the heterozygous mutations c.815G > A (p.R272Q) or c.1348C > T (p.R450C) in the RHOT1 gene encoding Miro1. Stem cell research 4 37364399
2018 Ectopic expression of Miro 1 ameliorates seizures and inhibits hippocampal neurodegeneration in a mouse model of pilocarpine epilepsy. Biochemistry and cell biology = Biochimie et biologie cellulaire 4 29365285
2025 MIRO1 Is Required for Dynamic Increases in Mitochondria-ER Contact Sites and Mitochondrial ATP During the Cell Cycle. Cells 3 40214436
2025 A substrate-interacting region of Parkin directs ubiquitination of the mitochondrial GTPase Miro1. The Journal of cell biology 3 40576561
2025 Restoration of Miro1's N-terminal GTPase function alleviates prenatal stress-induced mitochondrial fission via Drp1 modulation. Cell communication and signaling : CCS 2 40176126
2025 MIRO1 mutation leads to metabolic maladaptation resulting in Parkinson's disease-associated dopaminergic neuron loss. NPJ systems biology and applications 2 40246848
2025 RHOT1‑mediated molecular mechanism of mitochondrial dysfunction and its phenotypic effects on gastric cancer cells. International journal of oncology 2 41070627
2023 Generation of two induced pluripotent stem cell lines and the corresponding isogenic controls from Parkinson's disease patients carrying the heterozygous mutations c.1290A > G (p.T351A) or c.2067A > G (p.T610A) in the RHOT1 gene encoding Miro1. Stem cell research 2 37003181
2021 Epithelial Ablation of Miro1/Rhot1 GTPase Augments Lung Inflammation by Cigarette Smoke. Pathophysiology : the official journal of the International Society for Pathophysiology 2 35366248
2026 Geum japonicum Thunb. var. Chinese-P.decorata H.Andres herbal pair ameliorates CIRI-induced neuronal injury by facilitating mitochondrial transfer via the CD38/Miro1 signaling pathway. Phytomedicine : international journal of phytotherapy and phytopharmacology 1 41678910
2025 MIRO1 controls energy production and proliferation of vascular smooth muscle cells. bioRxiv : the preprint server for biology 1 39185180
2025 Miro1- a key player in β-cell function and mitochondrial dynamics under diabetes mellitus. Mitochondrion 1 40204078
2025 Death-Associated Protein 3 Triggers Intrinsic Apoptosis via Miro1 Upon Inducing Intracellular Calcium Changes. MedComm 1 40351389
2025 Miro1 knockout inhibits mouse breast cancer tumorigenesis. bioRxiv : the preprint server for biology 1 40654669
2025 Cross-Species Transcriptomic Integration Reveals a Conserved, MIRO1-Mediated Macrophage-to-T Cell Signaling Axis Driving Immunosuppression in Glioma. bioRxiv : the preprint server for biology 1 41292883
2023 Deletion of Miro1 in airway club cells potentiates allergic asthma phenotypes. Frontiers in allergy 1 37377691
2026 MIRO1-mediated mitochondrial fusion is required for stomatal immunity in Arabidopsis. Nature plants 0 41644634
2026 Miro1 in Parkinson's Disease: A Key Regulator of Mitochondrial Homeostasis and Neurodegeneration. Neuromolecular medicine 0 41792389
2026 Dihuang Yinzi ameliorates post-stroke depression through Miro1 ubiquitination-dependent mitophagy. Journal of ethnopharmacology 0 41850637
2026 Miro1 Mediates the Neuroprotective Effects of Electroacupuncture Against Cerebral Ischemia-Reperfusion Injury in Mice. Journal of integrative neuroscience 0 41914243
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2025 Miro1 Mediates Skeletal Muscle Insulin Resistance in Type 2 Diabetes. medRxiv : the preprint server for health sciences 0 41030931
2025 Miro1 protects against brain injury after CPR in rats by enhancing the effect of BMSCs on mitochondrial homeostasis. Stem cell research & therapy 0 41153049
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