Affinage

RHOT1

Mitochondrial Rho GTPase 1 · UniProt Q8IXI2

Length
618 aa
Mass
70.8 kDa
Annotated
2026-06-10
99 papers in source corpus 40 papers cited in narrative 40 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

RHOT1/Miro1 is an outer mitochondrial membrane Rho-GTPase that functions as the master scaffold coupling mitochondria to cytoskeletal motors and thereby controls activity-dependent organelle positioning at sites of high energy demand (PMID:19249275, PMID:28615318). Through GTPase-dependent recruitment of the TRAK adaptors (Grif-1/TRAK2, TRAK1), Miro1 links mitochondria to kinesin (KIF5) and dynein motors to drive bidirectional axonal and microtubule-based transport, with cryo-EM resolving TRAK1 docking at two sites spanning the nGTPase, EF-hand pairs, and cGTPase, and the first GTPase domain dictating transport directionality (PMID:19249275, PMID:19103291, PMID:24092329, PMID:24492963, PMID:40615373, PMID:32637409). Miro1 also serves as the mitochondrial receptor for the actin motor myosin XIX, binding its C-terminal tail in a GTPase-state-dependent manner and stabilizing the motor (PMID:30111583). Its two EF-hand calcium-binding domains act as cytosolic Ca2+ sensors that disrupt the Miro1/KIF5/tubulin complex to halt mitochondrial movement and drive a fission-independent mitochondrial shape transition required for mitophagy initiation, enabling repositioning of mitochondria at presynaptic terminals and astrocytic processes for homeostatic plasticity and Ca2+ signaling (PMID:19249275, PMID:29694881, PMID:28039205, PMID:26631479). Beyond transport, Miro1 organizes mitochondria-ER contact sites and mitochondrial Ca2+ handling, restrains MFN-mediated outer-membrane fusion under elevated Ca2+, and through splice variants and a transmembrane-domain interaction with Pex19 also localizes to peroxisomes to regulate their motility and Drp1-dependent fission (PMID:40214436, PMID:34431132, PMID:29222186, PMID:31894645). By positioning mitochondria peripherally, Miro1 establishes local ATP and H2O2 gradients that support actin dynamics, focal adhesion assembly, and cell migration (PMID:28615318, PMID:33341544). Miro1 is a direct substrate of the PINK1/Parkin mitophagy pathway: activated Parkin ubiquitylates Miro1 at multiple conserved lysines in a PINK1-Ser65-phosphorylation-dependent manner, with a conserved Parkin Ubl-RING0 linker region mediating the Miro1 interaction and rapid ubiquitination needed for Parkin recruitment to damaged mitochondria (PMID:24647965, PMID:40576561). Failure to remove Miro1 from depolarized mitochondria blocks mitophagy and is a common feature of Parkinson's disease patient cells, and the PD-associated EF-hand mutation R272Q impairs calcium buffering, disrupts bioenergetics and ER-mitochondria tethering, elevates α-synuclein, and causes dopaminergic neuron loss in iPSC and knock-in mouse models (PMID:31564441, PMID:32280985, PMID:36533136, PMID:39913247).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 2008 High

    Established how Miro1 physically engages the transport machinery, showing it recruits the TRAK/Grif-1 adaptor to mitochondria in a GTPase-dependent fashion to drive anterograde movement.

    Evidence Reciprocal co-IP, GTPase-domain mutants, and live neuronal imaging

    PMID:19103291

    Open questions at the time
    • Did not resolve the kinesin contact directly
    • Structural basis of adaptor recruitment unknown
  2. 2009 High

    Defined Miro1's central function as a Ca2+-gated linker between mitochondria and KIF5 kinesin, explaining how neuronal activity halts mitochondrial transport.

    Evidence EF-hand dominant-negative mutants, Co-IP with KIF5, live imaging under glutamate/NMDA stimulation

    PMID:19249275

    Open questions at the time
    • Molecular mechanism of Ca2+-induced complex disassembly not structurally resolved
    • Did not address retrograde/dynein engagement
  3. 2013 Medium

    Extended the adaptor complex, placing DISC1 with TRAK1 and Miro1 to specify anterograde transport and linking it to a disease variant.

    Evidence Co-IP of DISC1–TRAK1–Miro1 complex and live axon imaging

    PMID:24092329

    Open questions at the time
    • Single lab
    • Direct vs. indirect DISC1–Miro1 contact not distinguished
  4. 2014 High

    Identified Miro1 as a direct PINK1/Parkin mitophagy substrate, mapping the ubiquitylation sites and establishing PINK1-dependent Parkin activation as the trigger for its removal.

    Evidence In vitro E3 ligase reconstitution with recombinant Parkin/Miro1, mass spectrometry site mapping, mutagenesis

    PMID:24647965

    Open questions at the time
    • Did not define Parkin's Miro1-binding region
    • Cellular kinetics of removal not addressed
  5. 2014 High

    Demonstrated the physiological necessity of Miro1-directed transport in vivo, showing axonal mitochondrial depletion drives motor neuron disease while respiration and Ca2+ inhibition are preserved.

    Evidence Neuron-specific Miro1 knockout mice with axonal transport and respiratory assays

    PMID:25136135

    Open questions at the time
    • Separation of anterograde vs. retrograde roles incomplete
    • Cell-autonomous vs. circuit effects not fully dissected
  6. 2014 Medium

    Broadened Miro1's roles beyond neurons to dynein-based redistribution in lymphocytes and intercellular mitochondrial transfer from stem cells, indicating motor-coupling functions in immune and regenerative contexts.

    Evidence siRNA knockdown with dynein co-IP and migration assays; Miro1 gain/loss-of-function with mitochondrial transfer tracking and in vivo injury models

    PMID:24431222 PMID:24492963

    Open questions at the time
    • Single labs
    • Mechanism of intercellular transfer (tunneling nanotubes vs. vesicles) not resolved
  7. 2017 High

    Connected Miro1-dependent mitochondrial positioning to local energy supply, showing peripheral ATP gradients drive actin dynamics, focal adhesions, and cell migration.

    Evidence Miro1-/- MEFs with ATP:ADP biosensor, focal adhesion imaging, migration assays

    PMID:28615318

    Open questions at the time
    • Did not establish the redox component
    • Generalizability beyond fibroblasts untested
  8. 2017 Medium

    Showed Miro1 levels are pathologically degraded in disease, with ALS mutant SOD1 lowering Miro1 via PINK1/Parkin (not Ca2+) to impair axonal transport.

    Evidence ALS-SOD1 transfection in cortical/motor neurons, Miro1 quantification, rescue by Miro1 OE or PINK1 ablation

    PMID:28973175

    Open questions at the time
    • Single lab
    • Direct link to motor neuron death in vivo not shown
  9. 2018 High

    Expanded the motor repertoire by identifying Miro1 as the GTPase-state-regulated mitochondrial receptor for the actin motor myosin XIX, with motor stability dependent on Miro1.

    Evidence Proximity labeling, direct pulldown binding assays, in vivo recruitment, GTPase mutants

    PMID:30111583

    Open questions at the time
    • Functional consequence of actin-based transport in vivo limited
    • Coordination with microtubule motors unresolved
  10. 2018 High

    Resolved Miro1's EF-hand-driven mechanism for a fission-independent mitochondrial shape transition (MiST) required for mitophagy, and linked Miro1 to Ca2+ uptake machinery via the MCU complex.

    Evidence EF-hand mutagenesis with Ca2+ manipulation and mitophagy assays; MCU N-terminal domain mapping with co-IP and transport assays

    PMID:29686046 PMID:29694881

    Open questions at the time
    • Structural basis of MiST not defined
    • MCU–Miro1 interaction single lab
  11. 2018 High

    Defined Miro1's dual-organelle role, showing splice variants and a transmembrane Pex19 interaction target Miro1 to peroxisomes to drive their microtubule-based motility via TRAK2.

    Evidence Splice variant characterization, Pex19 interaction studies, knockdown/re-expression, live peroxisome tracking and modelling

    PMID:29222186 PMID:29364559

    Open questions at the time
    • Relative contribution of variants vs. transmembrane targeting partly overlapping
    • Regulation of organelle choice unknown
  12. 2016 High

    Showed Miro1's EF-hand Ca2+ sensing controls activity-dependent mitochondrial positioning at synapses and in astrocytic processes, coupling organelle placement to local Ca2+ signaling and homeostatic plasticity.

    Evidence EF-hand mutant neurons and astrocytes with genetically encoded Ca2+ indicators, live imaging, electrophysiology in slices

    PMID:26631479 PMID:28039205

    Open questions at the time
    • Molecular targets downstream of repositioning incomplete
    • In vivo circuit consequences not addressed
  13. 2019 High

    Established defective Miro1 removal as a convergent Parkinson's disease feature, with PINK1, Parkin, and LRRK2 required for its clearance and a small molecule rescuing mitophagy and neurodegeneration.

    Evidence Patient fibroblast depolarization assays, iPSC neurons, Drosophila PD models, small-molecule screen

    PMID:31564441

    Open questions at the time
    • Mechanism of LRRK2 involvement not detailed
    • Clinical translation of small molecule untested
  14. 2019 Medium

    Linked RHOT1 coding mutations to PD pathophysiology through reduced ER-mitochondria contacts and disrupted Ca2+ homeostasis in patient cells.

    Evidence Patient fibroblast live imaging, MERC immunocytochemistry, Ca2+ and mitophagy assays

    PMID:31303019

    Open questions at the time
    • Single lab
    • Cell-type specificity (fibroblast vs. neuron) discrepancies
  15. 2020 Medium

    Deepened the regulatory and functional map: Miro1 restrains MFN-mediated fusion under Ca2+, peripheral positioning shapes H2O2 redox gradients for focal adhesions, and a PINK1-regulated Ser156 phosphorylation tunes Miro1 stability and degradation.

    Evidence Co-IP/BioID with EF-hand mutants for MFN; Miro1-/- MEFs with HyPer7 redox biosensor; CRISPR S156A iPSC dopaminergic neurons with respirometry

    PMID:33341544 PMID:34431132 PMID:35455950

    Open questions at the time
    • Single labs
    • Kinase responsible for Ser156 not definitively assigned
  16. 2020 Medium

    Modeled the PD-associated EF-hand mutation R272Q, showing it impairs calcium buffering, disrupts MERCs and autophagic flux, and impairs dopaminergic mitochondrial function.

    Evidence Isogenic CRISPR R272Q iPSC dopaminergic neurons with Ca2+ imaging, respirometry, mitophagy and neurotransmitter assays

    PMID:32280985 PMID:36533136

    Open questions at the time
    • Single lab
    • Mechanistic basis of opposite MERC change in neurons vs. fibroblasts unresolved
  17. 2020 High

    Provided the first high-resolution structural view, capturing the N-terminal GTPase domain bound to GTP in a non-catalytic state and modeling the intact protein as a crescent assembly.

    Evidence 1.7 Å X-ray crystallography (PDB 6D71) and SAXS

    PMID:33132189

    Open questions at the time
    • Full-length membrane-anchored structure absent
    • Functional consequence of GTP non-catalytic state unclear
  18. 2023 Medium

    Identified a VDAC-1 interaction at the outer membrane (in the C. elegans ortholog) coupling Miro1 to mitochondrial membrane potential.

    Evidence Co-IP and point mutagenesis (MIRO-1 E473G, VDAC-1 K163) with membrane potential measurements in C. elegans

    PMID:37306041

    Open questions at the time
    • Ortholog system
    • Human relevance and mechanism of potential maintenance untested
  19. 2025 High

    Resolved the architecture of the Miro1–TRAK1 transport complex and the biochemical basis of Parkin recruitment, defining two TRAK1 docking sites and an essential Parkin Ubl-RING0 linker for Miro1 ubiquitination.

    Evidence Cryo-EM of MIRO1–TRAK1 with mutagenesis and localization assays; recombinant interaction and ubiquitination assays mapping the Parkin linker

    PMID:40576561 PMID:40615373

    Open questions at the time
    • Full motor-complex (kinesin/dynein) architecture not resolved
    • How Ca2+ remodels these interfaces structurally unaddressed
  20. 2025 High

    Provided in vivo disease causality for the EF-hand mutation, with R272Q/R285Q knock-in mice and patient iPSC neurons showing oxidative stress, bioenergetic failure, calpain-dependent α-synuclein cleavage, and dopaminergic neuron loss.

    Evidence iPSC midbrain organoids/neurons with isogenic controls and Miro1 p.R285Q knock-in mice with metabolic, Ca2+, calpain, and histological assays

    PMID:39913247

    Open questions at the time
    • Mechanistic link from calpain activation to α-synuclein pathology incomplete
    • Therapeutic targeting not tested
  21. 2025 Medium

    Extended Miro1 function to cell-cycle and proliferative control, showing it drives dynamic MERC formation (via GRP75) and cristae/ETC integrity required for G1/S progression in fibroblasts and vascular smooth muscle.

    Evidence Fibroblast and smooth-muscle Miro1 KO, proximity-ligation/split-GFP MERC assays, domain mutants, cristae EM and ETC activity assays (one preprint)

    PMID:39185180 PMID:40214436

    Open questions at the time
    • One source is a preprint
    • EF-hand-independent cristae role mechanistically undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How Ca2+ binding to the EF-hands is structurally transmitted to remodel motor-adaptor interfaces, and how Miro1 dynamically partitions its scaffolding among kinesin, dynein, myosin XIX, MERC, and mitophagy functions, remain unresolved.
  • No full-length membrane-anchored structure with bound motors
  • Mechanism coordinating competing scaffold functions unknown
  • Regulation of organelle (mitochondria vs. peroxisome) and motor selection undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003924 GTPase activity 5 GO:0060090 molecular adaptor activity 5 GO:0140299 molecular sensor activity 5 GO:0008092 cytoskeletal protein binding 4
Localization
GO:0005739 mitochondrion 4 GO:0005777 peroxisome 3
Pathway
R-HSA-5653656 Vesicle-mediated transport 4 R-HSA-1643685 Disease 3 R-HSA-9609507 Protein localization 3 R-HSA-9612973 Autophagy 3 R-HSA-1640170 Cell Cycle 1
Partners
KIF5MCUMFNMYO19PARK2PINK1TRAK1TRAK2
Complex memberships
MCU complexMIRO1–TRAK1 transport complex

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 Miro1 physically links mitochondria to KIF5 kinesin motor proteins, enabling microtubule-based transport. Ca2+ binding to Miro1's EF-hand domains (at micromolar levels) inhibits this linkage, halting mitochondrial movement. Mutation of EF-hand domains to prevent Ca2+ binding blocked glutamate/NMDA receptor-induced mitochondrial stopping but preserved basal motility. Dominant-negative EF-hand mutant expression, live-cell imaging, neuronal activity manipulation (glutamate/NMDA stimulation), Co-IP of Miro1 with KIF5 Neuron High 19249275
2008 Miro1 recruits the adaptor protein Grif-1 (TRAK2) to mitochondria in a GTPase-dependent manner. This Miro1–Grif-1 complex promotes anterograde transport of mitochondria into neuronal processes. Mutation of Miro1's first GTPase domain impairs Grif-1 recruitment and alters mitochondrial distribution and morphology. Co-IP, overexpression/dominant-negative constructs, live neuronal imaging, subcellular fractionation Molecular and cellular neurosciences High 19103291
2014 Miro1 knockout in mice depletes mitochondria from corticospinal tract axons and causes progressive upper motor neuron disease and developmental defects in cranial motor nuclei. Miro1-deficient neurons show defective retrograde axonal mitochondrial transport but retain normal mitochondrial respiratory function and Ca2+-mediated inhibition of movement. Neuron-specific Miro1 knockout mice, immunofluorescence, neurological behavioral analysis, axonal transport assays Proceedings of the National Academy of Sciences of the United States of America High 25136135
2014 Parkin ubiquitylates Miro1 at conserved lysine residues (K153, K230, K235, K330, K572) in a PINK1 phosphorylation-dependent manner. PINK1 phosphorylation of Parkin at Ser65 is required for substrate (Miro1) ubiquitylation. Miro1 serves as a direct substrate of activated Parkin E3 ligase. In vitro E3 ligase reconstitution assay with recombinant full-length untagged Parkin and Miro1, mass spectrometry identification of ubiquitylation sites, mutagenesis of Parkin catalytic cysteine and disease variants Open biology High 24647965
2017 Miro1 deletion in mouse embryonic fibroblasts restricts mitochondria to the perinuclear area, depleting peripheral ATP:ADP ratios, and thereby impairs actin dynamics, lamellipodia protrusion, focal adhesion assembly/stability, and cell migration (both collective and single-cell). Miro1-/- MEF cells, genetically encoded ATP:ADP biosensor (PercevalHR), live-cell imaging, focal adhesion immunofluorescence, migration assays Molecular biology of the cell High 28615318
2013 DISC1 forms a complex with TRAK1 (trafficking kinesin-binding protein 1) and Miro1 on mitochondria and specifically promotes anterograde axonal mitochondrial transport. A rare DISC1 variant (37W) impairs anterograde transport and redistributes mitochondrial DISC1. Co-IP (DISC1–TRAK1–Miro1 complex), live neuronal axon imaging, disease-variant functional analysis Human molecular genetics Medium 24092329
2014 Miro1 regulates intercellular mitochondrial transfer from mesenchymal stem cells (MSC) to epithelial cells. Miro1 overexpression in MSC enhances mitochondrial transfer and therapeutic rescue of epithelial injury; Miro1 knockdown reduces transfer efficacy. Miro1 overexpression/knockdown in MSC, fluorescent mitochondria tracking, mouse models of airway injury and allergic inflammation The EMBO journal Medium 24431222
2014 Miro-1 associates with the dynein motor complex on lymphocyte mitochondria, and Miro-1 silencing impairs mitochondrial redistribution to the MTOC during chemokine CXCL12-induced polarization, reducing myosin II activation and actin polymerization, thereby impairing lymphocyte adhesion and migration. Miro-1 siRNA knockdown, co-IP with dynein, live-cell imaging, flow adhesion assays Molecular and cellular biology Medium 24492963
2017 ALS mutant SOD1 reduces endogenous Miro1 protein levels through PINK1/Parkin-dependent degradation (not via elevated cytosolic Ca2+), causing impaired anterograde axonal mitochondrial transport. Miro1 overexpression or PINK1 ablation rescues this transport deficit. ALS mutant SOD1 transfection in cortical and motor neurons, Miro1 protein level quantification, mitochondrial transport imaging, Parkin-dependence shown by co-expression experiments, Ca2+ measurements Human molecular genetics Medium 28973175
2018 Miro1 and Miro2 are identified as mitochondrial receptors for myosin XIX (Myo19). Miro1 binds directly to the C-terminal tail of Myo19, recruits it to mitochondria in vivo, and this recruitment is regulated by the GTPase state of Miro1's N-terminal Rho-GTPase domain. Myo19 protein stability depends on its association with Miro1/2. Proximity labeling, direct binding assays (pulldown), in vivo recruitment assays, Miro1/2 knockdown and overexpression, protein stability analysis Journal of cell science High 30111583
2018 Miro1, through its EF-hand domain 1, senses cytosolic Ca2+ elevation and mediates a distinct mitochondrial shape transition (MiST) that is independent of classical fission or swelling. Ca2+-dependent disruption of the Miro1/KIF5B/tubulin complex is controlled by the EF1 domain. Miro1-dependent MiST is required for autophagy/mitophagy initiation. EF-hand mutant expression, live-cell Ca2+ manipulation, GPCR activation, morphometric analysis, Miro1 KO cells, autophagy/mitophagy assays Cell reports High 29694881
2016 Miro1 Ca2+-sensing (EF-hand) function is required for activity-dependent repositioning of mitochondria to presynaptic terminals during prolonged neuronal activity. This repositioning decreases presynaptic Ca2+ signals and neurotransmitter release, enabling homeostatic plasticity. Miro1 EF-hand mutant neurons, genetically encoded presynaptic Ca2+ indicator SyGCaMP5, live imaging, electrophysiology EMBO reports High 28039205
2015 Miro1 Ca2+-sensing EF-hand domains regulate activity-dependent mitochondrial confinement in astrocytic processes near synapses. Miro1-mediated mitochondrial positioning reciprocally regulates intracellular Ca2+ signaling levels in astrocytic processes. EF-hand mutant Miro1 expression, live-cell confocal microscopy in rat organotypic hippocampal slices, Ca2+ imaging The Journal of neuroscience High 26631479
2017 Three splice variants of human Miro1 (var2, var3, var4) containing sequence insertions upstream of the transmembrane domain localize to peroxisomes, recognized by the cytosolic receptor Pex19. Peroxisomal Miro1 variants act as adaptors linking peroxisomes to TRAK2-containing microtubule transport complexes, promoting long-range peroxisome movement. Identification and characterization of splice variants, peroxisome localization by immunofluorescence, Pex19 interaction studies, MIRO1 knockdown/re-expression, live-cell peroxisome tracking The Journal of cell biology High 29222186
2018 Miro1 localizes to peroxisomes (in addition to mitochondria) and regulates microtubule-dependent peroxisome motility. Miro1's transmembrane domain mediates interaction with the peroxisomal membrane chaperone Pex19. Miro1-mediated pulling forces contribute to peroxisome membrane elongation and proliferation. Microscopy, live-cell imaging, mathematical modelling, peroxisome-targeted Miro1 fusion protein, Miro1 knockdown Traffic Medium 29364559
2019 In Parkinson's disease patient fibroblasts (>94%), Miro1 fails to be removed from depolarized mitochondria, blocking initiation of mitophagy. PINK1, Parkin, and LRRK2 are required molecular helpers for Miro1 removal from dysfunctional mitochondria. A small molecule that reduces Miro1 levels repairs this defect and rescues locomotor deficits and dopaminergic neurodegeneration in patient-derived neurons and fly PD models. Biochemical Miro1 depolarization assay in patient fibroblasts, iPSC-derived neurons, Drosophila PD models, small molecule screen Cell metabolism High 31564441
2019 RHOT1 mutations in PD patients (het c.815G>A; het c.1348C>T) reduce mitochondrial-ER contact sites (MERCs) and disrupt Ca2+ homeostasis in patient-derived fibroblasts, impairing energy metabolism and increasing mitophagy. Patient fibroblast live-cell imaging, immunocytochemistry for MERCs, Ca2+ homeostasis assays, mitophagy quantification Antioxidants & redox signaling Medium 31303019
2020 Miro1 Ser156 phosphorylation is a PINK1-regulated modification affecting Miro1 steady-state protein levels and degradation during mitophagy. A phospho-null S156A mutation causes significant depletion of Miro1 protein, impairs further degradation upon mitophagy induction, leads to slightly elongated mitochondria, and reduces mitochondrial oxygen consumption with depletion of OXPHOS complexes III and V in human dopaminergic neurons. CRISPR/Cas9 gene-edited iPSC (homozygous S156A), differentiation to dopaminergic neurons, mitophagy induction (CCCP), immunoblotting, Seahorse respirometry, live-cell mitochondrial movement imaging Cells Medium 35455950
2020 DISC1 promotes anterograde mitochondrial transport in a manner dependent on Miro1's GTP-bound (active) state at the first GTPase domain. The first GTPase domain of Miro1 determines the direction of mitochondrial transport. Miro1 GTPase domain mutants, live neuronal imaging, DISC1 co-expression experiments Frontiers in cell and developmental biology Medium 32637409
2020 Miro1 interacts with Mitofusin (MFN) and inhibits MFN-mediated mitochondrial outer membrane fusion in response to elevated mitochondrial Ca2+ concentration. This inhibition requires Miro1's EF-hand domain 1. Lowering mitochondrial Ca2+ or knocking down Miro1/2 promotes network fusion. Co-IP, proximity labeling proteomics (BioID), EF-hand mutant expression, ectopic MFN expression, MCU inhibitor treatment, Miro1/2 knockdown Journal of cellular biochemistry Medium 34431132
2020 Miro1 deletion in Miro1-/- MEFs restricts subcellular H2O2 to the perinuclear area and prevents peripheral oxidation of cytosolic peroxiredoxin 2 (PRX2) after mitochondrial complex I inhibition. Local H2O2 levels correlate with focal adhesion size and abundance; Miro1-/- cells have smaller focal adhesions with reduced vinculin and p130Cas phosphorylation. Miro1-/- MEFs, genetically encoded H2O2 biosensor HyPer7, PRX2/PRX3 oxidation state, focal adhesion immunofluorescence, rotenone treatment Redox biology Medium 33341544
2018 Mitochondrial calcium uniporter (MCU) interacts with Miro1 through MCU's N-terminal domain, which traverses the outer mitochondrial membrane. This MCU–Miro1 interaction is required for Miro1-directed mitochondrial movement; Miro1 is a novel component of the MCU complex. Co-IP, domain deletion/mutation of MCU N-terminus, mitochondrial transport imaging in neurons, MCU overexpression/knockdown The Journal of neuroscience Medium 29686046
2020 Miro1-mutant neurons (R272Q) show increased MERC number (vs. decreased in fibroblasts), altered mitochondrial dynamics, increased sensitivity to Ca2+ stress, reduced mitochondrial clearance, and blocked autophagic flux, indicating that mutant Miro1 disrupts ER-mitochondrial tethering and autophagic flux in neurons. iPSC-derived PD patient neurons (Miro1-R272Q), live-cell imaging, immunocytochemistry for MERCs, mitophagy assays, western blotting for autophagy markers Human molecular genetics Medium 32280985
2020 Peroxisomal fission is negatively regulated by Miro1 and Miro2 via suppression of Drp1-dependent fission, shared with their function on mitochondria. Peroxisomal targeting of Miro is regulated by the first GTPase domain and is mediated through an interaction of its transmembrane domain with the peroxisomal membrane protein chaperone Pex19. Miro1/2 KO cells, Drp1 dependence assays, Pex19 interaction studies, peroxisome morphology analysis by microscopy EMBO reports Medium 31894645
2020 Crystal structure of the human Miro1 N-terminal GTPase domain (1.7Å) reveals it bound to GTP in a non-catalytic configuration. Two conserved surfaces ('SELFYY' and 'ITIP' motifs) are identified as potential dimerization or binding partner interfaces. SAXS data model the intact soluble HsMiro1/2 as a crescent-shaped assembly. X-ray crystallography (1.7Å, PDB 6D71), SAXS of intact soluble domain Journal of structural biology High 33132189
2023 MIRO-1 (C. elegans ortholog) interacts with VDAC-1 at the outer mitochondrial membrane; this interaction depends on residue E473 of MIRO-1 and K163 of VDAC-1. The MIRO-1 E473G point mutation disrupts this interaction and reduces mitochondrial membrane potential. Co-IP, point mutagenesis (E473G in MIRO-1, K163 in VDAC-1), mitochondrial membrane potential measurements in C. elegans EMBO reports Medium 37306041
2022 PD-associated Miro1 R272Q mutation (located in the first EF-hand/calcium-binding domain) causes mitochondrial fragmentation, reduced cristae and ATP5A, impaired mitochondrial calcium buffering (phenocopied by MCU inhibition), reduced mitochondrial respiration, and defective dopamine neurotransmitter regulation via monoamine oxidase in dopaminergic neurons. CRISPR gene-edited iPSC (heterozygous R272Q), iPSC-derived dopaminergic neurons, mitophagy assays (CCCP), Ca2+ imaging (Thapsigargin), Seahorse respirometry, catecholamine neurotransmitter assays Frontiers in molecular neuroscience Medium 36533136
2022 The formin mDia2 stabilizes MIRO1 protein in cancer-associated fibroblasts. Loss of mDia2 or MIRO1 reduces peripheral mitochondrial positioning, lowers peripheral ATP levels and CAF-tumor contact-site ATP, causes metabolic dysfunction, and suppresses secretion of protumorigenic proteins, implicating an activin A–mDia2–MIRO1 axis in CAF function. mDia2/MIRO1 knockdown in fibroblasts and CAFs, mitochondrial localization imaging, ATP biosensor, proteomic secretome analysis, in vivo tumor models Cancer research Medium 35997559
2025 Cryo-EM structure of the MIRO1–TRAK1 complex reveals TRAK1 binds MIRO1 at two distinct sites: TRAK1(569-623) binds in a cleft between the nGTPase and first EF-hand pair; TRAK1(425-428) binds a pocket between the second EF-hand pair and cGTPase. The complex dimerizes via interactions through the second EF-hand pair and cGTPase. Both sites are required for TRAK1 mitochondrial localization, validated by mutagenesis and binding assays. Cryo-EM structure determination, mutagenesis of both binding sites, 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 is indispensable for Parkin–Miro1 interaction and is required for Miro1 ubiquitination. This linker region explains fast kinetics of Miro1 ubiquitination and provides a biochemical basis for Miro1-dependent Parkin recruitment to the outer mitochondrial membrane prior to activation. Recombinant protein interaction assays, mutagenesis of Parkin linker region, in vitro ubiquitination assays, cellular Parkin recruitment assays The Journal of cell biology High 40576561
2025 Patient-derived iPSC neurons and knock-in mice expressing Miro1 p.R272Q (murine orthologue p.R285Q) show increased oxidative stress, disrupted mitochondrial bioenergetics, elevated α-synuclein levels, calcium-dependent calpain activation with α-synuclein cleavage, and significant dopaminergic neuron loss with phospho-α-synuclein accumulation in striatum. iPSC-derived midbrain organoids and dopaminergic neurons (isogenic controls), Miro1 p.R285Q knock-in mice, metabolic assays, Ca2+ measurements, calpain activity assays, immunohistochemistry, behavioral analysis Brain : a journal of neurology High 39913247
2025 Miro1 accumulates in skeletal muscle of obese/T2D mice and humans due to impaired insulin-mediated AKT–Miro1 interaction at the outer mitochondrial membrane. Muscle-specific Miro1 deletion improves insulin action and mitochondrial oxidative capacity. Exercise training reduces skeletal muscle Miro1 accumulation in T2D patients, correlating with improved insulin sensitivity. Human clinical exercise intervention (randomized, N=24 T2D patients), muscle-specific Miro1 KO mice, AKT-Miro1 interaction assays, metabolic/insulin sensitivity measurements, Seahorse respirometry medRxivpreprint Medium 41030931
2025 MIRO1 maintains mitochondrial cristae integrity and ETC complex I activity and super-complex formation in vascular smooth muscle cells (VSMCs), enabling PDGF-stimulated ATP production for G1/S cell-cycle progression. A MIRO1 mutant lacking EF hands (Ca2+-sensing) only partially rescues these effects, indicating that both mitochondrial positioning (EF-hand-dependent) and cristae integrity (EF-hand-independent) contribute to VSMC proliferation. Smooth-muscle-specific Miro1 KO mice, VSMC KD, mitochondrial cristae electron microscopy, ETC complex activity assays, cell-cycle analysis, ATP measurements, human coronary artery VSMC knockdown bioRxivpreprint Medium 39185180
2025 MIRO1 is required for dynamic increases in mitochondria-ER contact sites (MERCs) during G1/S cell-cycle progression. MIRO1 interacts with GRP75 (detected by proximity-ligation assay with VDAC1-IP3R at MERCs). MIRO1 EF-hand and transmembrane domain mutants fail to rescue cell proliferation or MERC formation. MIRO1 deficiency blocks G1/S transition and impairs ER Ca2+ release and mitochondrial Ca2+ uptake. Fibroblast-specific Miro1 KO, proximity-ligation assay, split-GFP ER/mitochondria contact assay, mitochondrial Ca2+/ATP measurements, MIRO1 domain mutants, cell cycle analysis Cells Medium 40214436
2016 In Xenopus embryos, the mitochondrial GTPase Rhot1 regulates microtubule-dependent mitochondrial trafficking required for aggregation of germinal granule components during primordial germ cell formation. Dominant-negative Rhot1ΔC (lacking transmembrane domain) inhibited germline-mitochondria aggregation and prevented germinal granule component aggregation, reducing PGC number. Dominant-negative Rhot1ΔC expression in Xenopus embryos, fluorescence imaging of germline mitochondria and germinal granules, PGC counting Development, growth & differentiation Medium 27585825
2022 Miro1 depletion in mouse oocytes via oocyte-specific KO disrupts mitochondrial spatial distribution (causing perinuclear and cortical aggregates) and reduces polar body extrusion by ~20%, implicating Miro1 as a mitochondrial adaptor setting mitochondrial distribution in oocytes. Oocyte-specific Miro1 conditional KO, live imaging of mitochondrial distribution, polar body extrusion quantification, embryo development in vitro Frontiers in cell and developmental biology Medium 36325364
2025 MIRO1 associates with cytoskeleton and cell cycle proteins (by mass spectrometry), regulates dynein motor for MTOC dynamics at the GV stage (determining meiotic resumption), and regulates Aurora A and KIF11 for meiotic spindle assembly in porcine and mouse oocytes. MIRO1 also interacts with DRP1, Parkin, and LAMP2 for mitochondrial dynamics and mitophagy during oocyte meiosis. Mass spectrometry, siRNA/morpholino knockdown, rescue by Miro1 mRNA injection, immunofluorescence of spindle/MTOC/mitochondria in mouse and porcine oocytes Science China. Life sciences Medium 39815032
2021 Miro1 conditional deletion in parvalbumin (PV+) interneurons in mice impairs Miro1-directed mitochondrial trafficking, alters mitochondrial distribution and axonal arborization of PV+ interneurons, increases hippocampal γ-oscillation frequency ex vivo, and promotes anxiolysis, without abolishing PV+ interneuron-mediated inhibition. Cre-mediated Miro1 KO in PV+ interneurons, live and fixed imaging, ex vivo hippocampal γ-oscillation recording, behavioral assays eLife Medium 34190042
2025 Miro1 N-terminal GTPase domain activity is required for ER-mitochondria contact (ERMC) formation in differentiating neurons. Glucocorticoid-induced downregulation of Miro1 impairs ERMC formation and increases Drp1 Ser616 phosphorylation (promoting fission). Miro1 overexpression restores ERMC formation, increases mitochondrial Ca2+ uptake, and reduces Drp1-Ser616 phosphorylation. AAV-mediated expression of Miro1 WT and N-terminal GTPase mutant (P26V) in hippocampal neurons of prenatally stressed mice, hiPSC-derived neurons, Drp1 phosphorylation analysis, ERMC imaging Cell communication and signaling Medium 40176126
2014 CK2β (regulatory subunit of Casein Kinase II) promotes PINK1-cytoplasmic isoform (PINK1-cyto)/Parkin-mediated degradation of Miro1, independent of CK2α. CK2β facilitates direct interaction between PINK1-cyto and Miro1 as shown by co-immunoprecipitation. HEK293 cell transfection, Western blot for Miro1 protein levels, co-immunoprecipitation Sheng wu yi xue gong cheng xue za zhi Low 25868250

Source papers

Stage 0 corpus · 99 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 547 19249275
2014 Miro1 regulates intercellular mitochondrial transport & enhances mesenchymal stem cell rescue efficacy. The EMBO journal 493 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 216 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 187 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) 177 29562677
2017 Miro1-mediated mitochondrial positioning shapes intracellular energy gradients required for cell migration. Molecular biology of the cell 144 28615318
2008 GTPase dependent recruitment of Grif-1 by Miro1 regulates mitochondrial trafficking in hippocampal neurons. Molecular and cellular neurosciences 140 19103291
2019 Miro1 Marks Parkinson's Disease Subset and Miro1 Reducer Rescues Neuron Loss in Parkinson's Models. Cell metabolism 130 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 116 24647965
2021 Circular RNA RHOT1 promotes progression and inhibits ferroptosis via mir-106a-5p/STAT3 axis in breast cancer. Aging 113 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 111 26631479
2016 Miro1-dependent mitochondrial positioning drives the rescaling of presynaptic Ca2+ signals during homeostatic plasticity. EMBO reports 108 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 102 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 89 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 80 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 72 31303019
2018 A role for Mitochondrial Rho GTPase 1 (MIRO1) in motility and membrane dynamics of peroxisomes. Traffic (Copenhagen, Denmark) 67 29364559
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 51 29686046
2019 Mitochondrial dysfunction is associated with Miro1 reduction in lung epithelial cells by cigarette smoke. Toxicology letters 50 31593750
2019 Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson's Disease Patients. Journal of clinical medicine 49 31888276
2014 Miro1: new wheels for transferring mitochondria. The EMBO journal 48 24711517
2017 New splicing variants of mitochondrial Rho GTPase-1 (Miro1) transport peroxisomes. The Journal of cell biology 47 29222186
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 46 33041957
2017 Inhibition of Miro1 disturbs mitophagy and pancreatic β-cell function interfering insulin release via IRS-Akt-Foxo1 in diabetes. Oncotarget 46 29207597
2020 Peroxisomal fission is modulated by the mitochondrial Rho-GTPases, Miro1 and Miro2. EMBO reports 40 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 32 32500352
2024 HMGB1 promotes mitochondrial transfer between hepatocellular carcinoma cells through RHOT1 and RAC1 under hypoxia. Cell death & disease 28 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 26 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
2020 Amyloid-beta oligomers induce Parkin-mediated mitophagy by reducing Miro1. The Biochemical journal 22 33155636
2022 A Protumorigenic mDia2-MIRO1 Axis Controls Mitochondrial Positioning and Function in Cancer-Associated Fibroblasts. Cancer research 21 35997559
2020 Insight into human Miro1/2 domain organization based on the structure of its N-terminal GTPase. Journal of structural biology 21 33132189
2025 The adaptor protein Miro1 modulates horizontal transfer of mitochondria in mouse melanoma models. Cell reports 20 39792553
2021 Miro1 functions as an inhibitory regulator of MFN at elevated mitochondrial Ca2+ levels. Journal of cellular biochemistry 19 34431132
2016 C. elegans miro-1 Mutation Reduces the Amount of Mitochondria and Extends Life Span. PloS one 18 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
2023 MIRO-1 interacts with VDAC-1 to regulate mitochondrial membrane potential in Caenorhabditis elegans. EMBO reports 14 37306041
2022 Miro1 R272Q disrupts mitochondrial calcium handling and neurotransmitter uptake in dopaminergic neurons. Frontiers in molecular neuroscience 14 36533136
2021 Miro1 Impairment in a Parkinson's At-Risk Cohort. Frontiers in molecular neuroscience 14 34434090
2025 Parkinson's disease mutant Miro1 causes mitochondrial dysfunction and dopaminergic neuron loss. Brain : a journal of neurology 13 39913247
2022 Miro1 depletion disrupts spatial distribution of mitochondria and leads to oocyte maturation defects. Frontiers in cell and developmental biology 13 36325364
2021 Propofol suppresses non-small cell lung cancer tumorigenesis by regulation of circ-RHOT1/miR-326/FOXM1 axis. Life sciences 13 33515563
2020 Precision Neurology for Parkinson's Disease: Coupling Miro1-Based Diagnosis With Drug Discovery. Movement disorders : official journal of the Movement Disorder Society 13 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
2025 Insufficient MIRO1 contributes to declined oocyte quality during reproductive aging. Science China. Life sciences 10 39815032
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
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 Structural-functional characterization of the MIRO1-TRAK1 complex. Nature communications 8 40615373
2025 Miro1: A potential target for treating neurological disorders. Neuroscience 7 40403957
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
2022 Interlinked role of ASN, TDP-43 and Miro1 with parkinopathy: Focus on targeted approach against neuropathy in parkinsonism. Ageing research reviews 7 36371014
2020 The role of RHOT1 and RHOT2 genetic variation on Parkinson disease risk and onset. Neurobiology of aging 7 32948353
2024 Miro1 improves the exogenous engraftment efficiency and therapeutic potential of mitochondria transfer using Wharton's jelly mesenchymal stem cells. Mitochondrion 5 38408618
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 Is Required for Dynamic Increases in Mitochondria-ER Contact Sites and Mitochondrial ATP During the Cell Cycle. Cells 4 40214436
2025 MIRO1 mutation leads to metabolic maladaptation resulting in Parkinson's disease-associated dopaminergic neuron loss. NPJ systems biology and applications 4 40246848
2025 A substrate-interacting region of Parkin directs ubiquitination of the mitochondrial GTPase Miro1. The Journal of cell biology 4 40576561
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 RHOT1‑mediated molecular mechanism of mitochondrial dysfunction and its phenotypic effects on gastric cancer cells. International journal of oncology 3 41070627
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 Death-Associated Protein 3 Triggers Intrinsic Apoptosis via Miro1 Upon Inducing Intracellular Calcium Changes. MedComm 2 40351389
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 Miro1 knockout inhibits mouse breast cancer tumorigenesis. bioRxiv : the preprint server for biology 1 40654669
2025 [Effects of electroacupuncture on cognitive impairment and mitophagy mediated by KIF5A/Miro1 pathway in Parkinson's disease mice]. Zhongguo zhen jiu = Chinese acupuncture & moxibustion 1 40825695
2025 Miro1 protects against brain injury after CPR in rats by enhancing the effect of BMSCs on mitochondrial homeostasis. Stem cell research & therapy 1 41153049
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 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
2026 Cross-species transcriptomic integration reveals a MIRO1-mediated macrophage-T cell axis in glioma. Life science alliance 0 42128668
2026 Dysfunction of the CD38-Miro1 Axis Disrupts Astrocyte-neuron Mitochondrial Transfer in Alzheimer's Disease: Mechanisms and Therapeutic Restoration. Journal of molecular neuroscience : MN 0 42184087
2026 Chemical modulation of Miro1 alleviates cell-type-specific vulnerabilities in Friedreich's ataxia. Cell chemical biology 0 42259290
2025 Miro1 Mediates Skeletal Muscle Insulin Resistance in Type 2 Diabetes. medRxiv : the preprint server for health sciences 0 41030931
2014 [CK2beta promotes Pink1/Parkin-mediated MIRO1 degradation]. Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi 0 25868250

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