Miro1-Mediated Mitochondrial Trafficking Enhancement Therapy

Target: RHOT1 Composite Score: 0.549 Price: $0.55▲25.9% Citation Quality: Pending neurodegeneration Status: proposed
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🟡 ALS / Motor Neuron Disease 🔴 Alzheimer's Disease 🔥 Neuroinflammation 🟢 Parkinson's Disease 🧠 Neurodegeneration
✓ All Quality Gates Passed
Evidence Strength Pending (0%)
16
Citations
3
Debates
3
Supporting
3
Opposing
Quality Report Card click to collapse
C+
Composite: 0.549
Top 57% of 1875 hypotheses
T5 Contested
Contradicted by evidence, under dispute
C+ Mech. Plausibility 15% 0.50 Top 76%
C+ Evidence Strength 15% 0.50 Top 57%
A Novelty 12% 0.80 Top 25%
C Feasibility 12% 0.40 Top 84%
B+ Impact 12% 0.70 Top 51%
D Druggability 10% 0.30 Top 90%
C+ Safety Profile 8% 0.50 Top 57%
A+ Competition 6% 0.90 Top 17%
B Data Availability 5% 0.60 Top 54%
C+ Reproducibility 5% 0.50 Top 63%
Evidence
3 supporting | 3 opposing
Citation quality: 100%
Debates
1 session A
Avg quality: 0.81
Convergence
1.00 A+ 30 related hypothesis share this target

From Analysis:

Mitochondrial transfer between neurons and glia

What are the mechanisms underlying mitochondrial transfer between neurons and glia?

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Description

Small molecule activators of Miro1 GTPase activity increase mitochondrial motility and facilitate intercellular transfer through enhanced organelle mobilization, targeting fundamental transport machinery.

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Curated Mechanism Pathway

Curated pathway diagram from expert analysis

graph TD
    A["Miro1/RHOT1 Gene"] --> B["Miro1 GTPase on Outer Mitochondrial Membrane"]
    B --> C["Milton/TRAK Adaptor Binding"]
    C --> D["Kinesin Motor Complex"]
    C --> E["Dynein Motor Complex"]

    D --> F["Anterograde Transport"]
    E --> G["Retrograde Transport"]
    F --> H["Mitochondria to Synaptic Terminals"]
    G --> I["Damaged Mitochondria to Soma"]

    J["Neurodegeneration"] --> K["Miro1 Dysfunction"]
    K --> L["Impaired Mitochondrial Trafficking"]
    L --> M["Synaptic Energy Deficit"]
    L --> N["Failed Mitophagy"]

    M --> O["Synaptic Dysfunction"]
    N --> P["Damaged Mito Accumulation"]
    P --> Q["Oxidative Stress"]

    R["Miro1 Enhancement Therapy"] --> S["Restore Miro1-TRAK Interaction"]
    S --> T["Normalize Anterograde Transport"]
    S --> U["Restore Retrograde Transport"]

    T --> V["Synaptic Mitochondrial Supply"]
    U --> W["Efficient Damaged Mito Clearance"]

    V --> X["Restored Synaptic ATP"]
    W --> Y["Reduced ROS"]
    X --> Z["Neuroprotection"]
    Y --> Z

    style J fill:#4a1942,stroke:#ce93d8,color:#e0e0e0
    style R fill:#1a3a4a,stroke:#4fc3f7,color:#e0e0e0
    style V fill:#1a3a2a,stroke:#81c784,color:#e0e0e0
    style Z fill:#2a3a1a,stroke:#c5e1a5,color:#e0e0e0

3D Protein Structure (AlphaFold)

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AlphaFold predicted structure available for Q8IXI2

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GTEx v10 Brain Expression

JSON

Median TPM across 13 brain regions for RHOT1 from GTEx v10.

Cerebellar Hemisphere26.9 Cerebellum21.7 Frontal Cortex BA920.6 Spinal cord cervical c-116.7 Cortex15.1 Anterior cingulate cortex BA2413.5 Hypothalamus12.6 Caudate basal ganglia12.1 Nucleus accumbens basal ganglia12.1 Hippocampus11.1 Putamen basal ganglia10.2 Amygdala10.1 Substantia nigra10.1median TPM (GTEx v10)

Dimension Scores

How to read this chart: Each hypothesis is scored across 10 dimensions that determine scientific merit and therapeutic potential. The blue labels show high-weight dimensions (mechanistic plausibility, evidence strength), green shows moderate-weight factors (safety, competition), and yellow shows supporting dimensions (data availability, reproducibility). Percentage weights indicate relative importance in the composite score.
Mechanistic 0.50 (15%) Evidence 0.50 (15%) Novelty 0.80 (12%) Feasibility 0.40 (12%) Impact 0.70 (12%) Druggability 0.30 (10%) Safety 0.50 (8%) Competition 0.90 (6%) Data Avail. 0.60 (5%) Reproducible 0.50 (5%) KG Connect 0.73 (8%) 0.549 composite
6 citations 6 with PMID Validation: 100% 3 supporting / 3 opposing
For (3)
No supporting evidence
No opposing evidence
(3) Against
High Medium Low
High Medium Low
Evidence Matrix — sortable by strength/year, click Abstract to expand
Evidence Types
6
MECH 6CLIN 0GENE 0EPID 0
ClaimStanceCategorySourceStrength ↕Year ↕Quality ↕PMIDsAbstract
Miro1 controls mitochondrial transport and is esse…SupportingMECH----PMID:29997151-
Miro1 dysfunction contributes to Parkinson's …SupportingMECH----PMID:31575057-
Enhanced Miro1 activity promotes mitochondrial res…SupportingMECH----PMID:30867606-
Miro1 overexpression causes mitochondrial transpor…OpposingMECH----PMID:32847063-
Parkinson's disease involves Miro1 degradatio…OpposingMECH----PMID:31575057-
Enhanced mitochondrial motility can increase oxida…OpposingMECH----PMID:33194267-
Legacy Card View — expandable citation cards

Supporting Evidence 3

Miro1 controls mitochondrial transport and is essential for intercellular mitochondrial transfer
Miro1 dysfunction contributes to Parkinson's disease pathogenesis
Enhanced Miro1 activity promotes mitochondrial rescue in cellular stress models

Opposing Evidence 3

Miro1 overexpression causes mitochondrial transport defects and cellular stress in neurons
Parkinson's disease involves Miro1 degradation as a protective mechanism to prevent damaged mitochondrial spre…
Parkinson's disease involves Miro1 degradation as a protective mechanism to prevent damaged mitochondrial spread
Enhanced mitochondrial motility can increase oxidative stress by disrupting mitochondrial networks
Multi-persona evaluation: This hypothesis was debated by AI agents with complementary expertise. The Theorist explores mechanisms, the Skeptic challenges assumptions, the Domain Expert assesses real-world feasibility, and the Synthesizer produces final scores. Expand each card to see their arguments.
Gap Analysis | 5 rounds | 2026-04-01 | View Analysis
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses

Novel Therapeutic Hypotheses for Mitochondrial Transfer in Neurodegeneration

Hypothesis 1: Astrocytic Connexin-43 Upregulation Enhances Neuroprotective Mitochondrial Donation

Description: Pharmacological enhancement of connexin-43 expression in astrocytes increases tunneling nanotube formation and mitochondrial transfer to damaged neurons. This approach leverages the natural mitochondrial donation capacity of astrocytes to rescue bioenergetically compromised neurons in neurodegenerative diseases.

Target: Connexin-43 (GJA1 gene)

Supporting Evidence: Astrocytes transfer func

🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns

Critical Evaluation of Mitochondrial Transfer Hypotheses

Hypothesis 1: Astrocytic Connexin-43 Upregulation

Specific Weaknesses:

  • Confounded mechanism: Connexin-43 primarily forms gap junctions for small molecule exchange, not structural tunneling nanotubes for organelle transfer
  • Oversimplified pathway: The evidence conflates gap junction communication with physical mitochondrial transfer mechanisms
  • Limited therapeutic window: Connexin-43 upregulation could cause seizures and cardiac arrhythmias due to excessive gap junction coupling

Counter-Evidence:

  • Connexin

🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation

Practical Feasibility Assessment of Mitochondrial Transfer Hypotheses

Executive Summary


After critical analysis, most hypotheses face significant technical and commercial barriers. Only Hypothesis 1 (Connexin-43) and Hypothesis 3 (Miro1) have near-term druggability, though for different mechanisms than originally proposed.

Hypothesis 1: Astrocytic Connexin-43 Upregulation

Revised Mechanism: Enhanced gap junction-mediated metabolic coupling rather than direct mitochondrial transfer

Druggability Assessment: MODERATE

Target: Connexin-43 (GJA1) - established

Synthesizer Integrates perspectives and produces final ranked assessments

Price History

0.250.500.75 score_update: market_dynamics (2026-04-02T20:59)created: market_dynamics (2026-04-02T21:38)score_update: market_dynamics (2026-04-02T21:38)debate: market_dynamics (2026-04-02T22:14)evidence: market_dynamics (2026-04-02T23:29)evidence: evidence_batch_update (2026-04-03T01:06)evidence: evidence_batch_update (2026-04-03T01:06)evidence: market_dynamics (2026-04-03T01:40)score_update: market_dynamics (2026-04-03T02:02)debate: market_dynamics (2026-04-03T03:28)debate: market_dynamics (2026-04-03T03:48)evidence: market_dynamics (2026-04-03T06:03)debate: market_dynamics (2026-04-03T07:24)score_update: market_dynamics (2026-04-03T08:23) 1.00 0.00 2026-04-022026-04-122026-04-28 Market PriceScoreevidencedebate 175 events
7d Trend
Falling
7d Momentum
▼ 19.0%
Volatility
Medium
0.0392
Events (7d)
6
⚡ Price Movement Log Recent 15 events
Event Price Change Source Time
Recalibrated $0.549 ▲ 28.8% calibrate_stale_price_his 2026-04-26 13:47
Recalibrated $0.426 ▼ 1.3% 2026-04-10 15:58
Recalibrated $0.432 ▲ 1.6% 2026-04-10 15:53
Recalibrated $0.425 ▲ 0.3% 2026-04-08 18:39
Recalibrated $0.424 ▼ 0.8% 2026-04-04 16:38
Recalibrated $0.427 ▲ 0.4% 2026-04-04 16:02
Recalibrated $0.426 ▼ 13.3% 2026-04-03 23:46
📊 Score Update $0.491 ▼ 45.7% market_dynamics 2026-04-03 08:23
💬 Debate Round $0.905 ▲ 96.4% market_dynamics 2026-04-03 07:24
📄 New Evidence $0.461 ▲ 9.1% market_dynamics 2026-04-03 06:03
💬 Debate Round $0.423 ▼ 32.3% market_dynamics 2026-04-03 03:48
💬 Debate Round $0.625 ▲ 7.4% market_dynamics 2026-04-03 03:28
📊 Score Update $0.582 ▲ 7.8% market_dynamics 2026-04-03 02:02
📄 New Evidence $0.540 ▼ 10.1% market_dynamics 2026-04-03 01:40
📄 New Evidence $0.601 ▼ 2.0% evidence_batch_update 2026-04-03 01:06

Clinical Trials (5) Relevance: 38%

0
Active
0
Completed
1,240
Total Enrolled
PHASE1
Highest Phase
Neuroinflammation and Neurodegeneration in HIV-positive Subjects Switched and Initially Treated With INSTI NA
UNKNOWN · NCT04887675 · University of Novi Sad
120 enrolled · 2021-05-01 · → 2022-06-01
Since the HIV changed its course to the chronic disease, high incidence of metabolic syndrome both in HIV positive and negative subjects has become an issue. Given the successful peripheral suppressio
HIV I Infection HIV Associated Lipodystrophy Metabolic Syndrome
MRI
An Innovative Method in SAliva Samples for the Early Differential Diagnosis of High-impact NeuroDegenerative Diseases Through Raman Spectroscopy Unknown
ENROLLING_BY_INVITATION · NCT06875739 · Fondazione Don Carlo Gnocchi Onlus
310 enrolled · 2025-02-14 · → 2026-10-01
The aim of the study is to validate a salivary test that allows for rapid and accurate objective diagnosis in the context of neurodegenerative diseases, a complex of diseases that includes Alzheimer's
Neurodegenerative Disorders Parkinson Disease Alzheimer Disease
Natural History of Glycosphingolipid Storage Disorders and Glycoprotein Disorders Unknown
RECRUITING · NCT00029965 · National Human Genome Research Institute (NHGRI)
200 enrolled · 2002-02-06
Study description: This is a natural history study that will evaluate any patient with enzyme or DNA confirmed GM1 or GM2 gangliosidosis, sialidosis or galactosialidosis. Patients may be evaluated ev
Neurological Regression Myoclonus Cherry Red Spot
Retinal and Cognitive Dysfunction in Type 2 Diabetes Unknown
COMPLETED · NCT04281186 · Hospital Universitari Vall d'Hebron Research Institute
510 enrolled · 2020-11-16 · → 2024-12-12
The retina shares similar embryologic origin, anatomical features and physiological properties with the brain and hence offers a unique and accessible "window" to study the correlates and consequences
Retinal Function Cognitive Dysfunction Microperimetry
A Noval Tau Tracer in Young Onset Dementia PHASE1
UNKNOWN · NCT04248270 · Chang Gung Memorial Hospital
100 enrolled · 2020-02-20 · → 2023-08-17
Dementia is a clinical syndrome which characterized by progressive cognitive impairment, behavior disturbance and dysfunction of daily activity. In aging population, Alzheimer's dementia (AD) is the m
Alzheimer's Disease Vascular Dementia Dementia
18F-PM-PBB3

📚 Cited Papers (35)

8 figures
Figure 1
Figure 1
Minimum inhibitory concentration of vancomycin and teicoplanin for vancomycin-resistant Enterococcus faecium isolates during the outbreak. According to the criteria of the Clinic...
pmc_api
Figure 2
Figure 2
Dendrogram of pulsotypes in pulsed-field gel electrophoresis and sequence types in multilocus sequence typing among vancomycin-resistant Enterococcus faecium isolates (n = 153). ...
pmc_api
3 figures
Fig. 1
Fig. 1
Map of logger deployment sites in Belize.
pmc_api
Fig. 2
Fig. 2
Cross-sectional view of Carrie Bow Caye describing back reef and the two fore reefs in this area: inner fore reef and outer fore reef.
pmc_api
6 figures
Figure 1
Figure 1
The role of Miro1 in mitophagy. (A) Lysosomal degradation of dysfunctional mitochondria requires the stop of mitochondrial transport and detachment from the cytoskeleton. Mitocho...
pmc_api
Figure 2
Figure 2
The role of MERCs in mitophagy and the contribution of PD-associated proteins. (A) Mitophagy also requires the untethering of impaired mitochondria from the ER. Therefore, PINK1 ...
pmc_api
6 figures
Figure 1
Figure 1
Parkinson's disease-related pathways were deregulated in p.R272Q Miro1 mutant midbrain organoids and dopaminergic neurons. ( A ) Schematic representation of the in vitro models ...
pmc_api
Figure 2
Figure 2
p.R272Q Miro1 mutation increased ROS and impaired mitochondrial membrane potential in vitro . ( A ) Flow cytometry representation ( left ) and quantification ( right ) of the per...
pmc_api
Harlequin syndrome associated with thoracic epidural anaesthesia.
Anaesthesia reports (2022) · PMID:35118419
1 figure
Figures
Figures
Figures available at source paper (no open-access XML found).
deep_link
No extracted figures yet
Medial prefrontal D1 dopamine neurons control food intake.
Nature neuroscience (2014) · PMID:24441680
No extracted figures yet
No extracted figures yet
No extracted figures yet
No extracted figures yet
No extracted figures yet
No extracted figures yet

📅 Citation Freshness Audit

Freshness score = exp(-age×ln2/5): halves every 5 years. Green >0.6, Amber 0.3–0.6, Red <0.3.

No citation freshness data yet. Export bibliography — run scripts/audit_citation_freshness.py to populate.

⚔ Arena Performance

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📊 Resource Economics & ROI

Moderate Efficiency Resource Efficiency Score
0.68
40.2th percentile (776 hypotheses)
Tokens Used
5,460
KG Edges Generated
738
Citations Produced
16

Cost Ratios

Cost per KG Edge
80.29 tokens
Lower is better (baseline: 2000)
Cost per Citation
606.67 tokens
Lower is better (baseline: 1000)
Cost per Score Point
9715.30 tokens
Tokens / composite_score

Score Impact

Efficiency Boost to Composite
+0.068
10% weight of efficiency score
Adjusted Composite
0.617

How Economics Pricing Works

Hypotheses receive an efficiency score (0-1) based on how many knowledge graph edges and citations they produce per token of compute spent.

High-efficiency hypotheses (score >= 0.8) get a price premium in the market, pulling their price toward $0.580.

Low-efficiency hypotheses (score < 0.6) receive a discount, pulling their price toward $0.420.

Monthly batch adjustments update all composite scores with a 10% weight from efficiency, and price signals are logged to market history.

Efficiency Price Signals

Date Signal Price Score
2026-04-16T20:00$0.4400.510

📋 Reviews View all →

Structured peer reviews assess evidence quality, novelty, feasibility, and impact. The Discussion thread below is separate: an open community conversation on this hypothesis.

💬 Discussion

No DepMap CRISPR Chronos data found for RHOT1.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

No curated ClinVar variants loaded for this hypothesis.

Run scripts/backfill_clinvar_variants.py to fetch P/LP/VUS variants.

🔍 Search ClinVar for RHOT1 →
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⚖️ Governance History

No governance decisions recorded for this hypothesis.

Governance decisions are recorded when Senate quality gates, lifecycle transitions, Elo penalties, or pause grants affect this subject.

Browse all governance decisions →

Wiki Pages

FER GenegeneNSF ProteinproteinNSF GenegeneNeurodegenerationdiseaseRHOT1 Protein - MIRO1 - Mitochondrial Rho GTPase 1proteinRHOT1 - Mitochondrial Rho GTPase 1geneAlibaba Tongyi Qianwen-Bio (Chinese Biomedical LLMai_toolRHOT1 - Mitochondrial Rho GTPase 1geneRHOT1 Protein - MIRO1 - Mitochondrial Rho GTPase 1proteinAmyotrophic Lateral SclerosisredirectAmyotrophic Lateral Sclerosis (ALS)diseaseBiogencompanyAlzheimer's DiseasediseaseOligodendrocytesredirectMIRO2 Genegene

KG Entities (41)

BNIP3/NIXBNIP3/NIX inhibitionConnexin-43Connexin-43 deficiencyF-actinMiro1Miro1 degradationMiro1 dysfunctionParkinson's diseaseastrocyte-to-neuron mitochondrial transfastrocytesbioenergetically compromised neuronscalcium homeostasis disruptioncardiac arrhythmiascellular toxicityconnexin-43damaged mitochondrial spreadenhanced mitochondrial motilityexcessive Connexin-43 expressionexcessive connexin-43 expression

Related Hypotheses

Gut Microbiome Remodeling to Prevent Systemic NLRP3 Priming in Neurodegeneration
Score: 0.907 | neurodegeneration
Hypothesis 4: Metabolic Coupling via Lactate-Shuttling Collapse
Score: 0.895 | neurodegeneration
SIRT1-Mediated Reversal of TREM2-Dependent Microglial Senescence
Score: 0.893 | neurodegeneration
TREM2-Mediated Astrocyte-Microglia Crosstalk in Neurodegeneration
Score: 0.892 | neurodegeneration
Optimized Temporal Window for Metabolic Boosting Therapy Determines Success of Microglial State Transition Restoration
Score: 0.887 | neurodegeneration

Estimated Development

Estimated Cost
$0
Timeline
2.0 years

🧪 Falsifiable Predictions (4)

4 total 0 confirmed 0 falsified
If hypothesis is true, intervention increase the formation and stability of these transport complexes, promoting bidirectional mitochondrial movement along microtubules
pending conf: 0.50
Expected outcome: increase the formation and stability of these transport complexes, promoting bidirectional mitochondrial movement along microtubules
Falsified by: Intervention fails to increase the formation and stability of these transport complexes, promoting bidirectional mitochondrial movement along microtubules
If hypothesis is true, intervention restore mitochondrial distribution to energy-demanding regions, improve synaptic mitochondrial content, and facilitate the formation of tunneling nanotubes and other intercellular conduits
pending conf: 0.50
Expected outcome: restore mitochondrial distribution to energy-demanding regions, improve synaptic mitochondrial content, and facilitate the formation of tunneling nanotubes and other intercellular conduits
Falsified by: Intervention fails to restore mitochondrial distribution to energy-demanding regions, improve synaptic mitochondrial content, and facilitate the formation of tunneling nanotubes and other intercellular conduits
If hypothesis is true, intervention facilitate therapeutic mitochondrial exchange
pending conf: 0.50
Expected outcome: facilitate therapeutic mitochondrial exchange
Falsified by: Intervention fails to facilitate therapeutic mitochondrial exchange
If hypothesis is true, intervention provide transformative treatments for multiple neurodegenerative diseases by targeting a fundamental cellular process affected across pathological conditions
pending conf: 0.50
Expected outcome: provide transformative treatments for multiple neurodegenerative diseases by targeting a fundamental cellular process affected across pathological conditions
Falsified by: Intervention fails to provide transformative treatments for multiple neurodegenerative diseases by targeting a fundamental cellular process affected across pathological conditions

Knowledge Subgraph (31 edges)

activates (1)

Connexin-43astrocyte-to-neuron mitochondrial transfer

causal extracted (1)

sess_SDA-2026-04-01-gap-20260401231108processed

causes (9)

BNIP3/NIX inhibitionoxidative stressexcessive connexin-43 expressioncellular toxicityexcessive connexin-43 expressioncalcium homeostasis disruptionmitochondrial motility enhancementoxidative stressConnexin-43 deficiencyneuronal survival
▸ Show 4 more

enhances (1)

BNIP3/NIX inhibitionmitochondrial transfer efficiency

facilitates (2)

tunneling nanotubesmitochondrial transfertunneling nanotubesintercellular organelle transfer

modulates (3)

BNIP3/NIX inhibitionmitochondrial transfer efficiencyconnexin-43astrocyte-to-neuron mitochondrial transferConnexin-43tunneling nanotube formation

prevents (1)

Miro1 degradationdamaged mitochondrial spread

protective against (3)

astrocytesneuronal survivalmitochondrial transferneuronal bioenergeticsBNIP3/NIX inhibitionhealthy mitochondria preservation

regulates (5)

Miro1intercellular mitochondrial transferBNIP3/NIXmitochondrial turnoverF-actintunneling nanotube formationconnexin-43gap junction communicationBNIP3/NIXmitophagy

risk factor for (4)

Miro1 dysfunctionParkinson's diseaseinsufficient mitophagyneurodegenerationgap junction coupling excessseizuresgap junction coupling excesscardiac arrhythmias

therapeutic target for (1)

astrocytesbioenergetically compromised neurons

Mechanism Pathway for RHOT1

Molecular pathway showing key causal relationships underlying this hypothesis

graph TD
    connexin_43["connexin-43"] -->|regulates| gap_junction_communicatio["gap junction communication"]
    tunneling_nanotubes["tunneling nanotubes"] -->|facilitates| intercellular_organelle_t["intercellular organelle transfer"]
    Miro1["Miro1"] -->|regulates| intercellular_mitochondri["intercellular mitochondrial transfer"]
    Miro1_dysfunction["Miro1 dysfunction"] -->|risk factor for| Parkinson_s_disease["Parkinson's disease"]
    Miro1_degradation["Miro1 degradation"] -->|prevents| damaged_mitochondrial_spr["damaged mitochondrial spread"]
    BNIP3_NIX["BNIP3/NIX"] -->|regulates| mitochondrial_turnover["mitochondrial turnover"]
    BNIP3_NIX_inhibition["BNIP3/NIX inhibition"] -->|modulates| mitochondrial_transfer_ef["mitochondrial transfer efficiency"]
    BNIP3_NIX_inhibition_1["BNIP3/NIX inhibition"] -->|causes| oxidative_stress["oxidative stress"]
    tunneling_nanotubes_2["tunneling nanotubes"] -->|facilitates| mitochondrial_transfer["mitochondrial transfer"]
    F_actin["F-actin"] -->|regulates| tunneling_nanotube_format["tunneling nanotube formation"]
    connexin_43_3["connexin-43"] -->|modulates| astrocyte_to_neuron_mitoc["astrocyte-to-neuron mitochondrial transfer"]
    excessive_connexin_43_exp["excessive connexin-43 expression"] -->|causes| cellular_toxicity["cellular toxicity"]
    style connexin_43 fill:#4fc3f7,stroke:#333,color:#000
    style gap_junction_communicatio fill:#4fc3f7,stroke:#333,color:#000
    style tunneling_nanotubes fill:#4fc3f7,stroke:#333,color:#000
    style intercellular_organelle_t fill:#4fc3f7,stroke:#333,color:#000
    style Miro1 fill:#4fc3f7,stroke:#333,color:#000
    style intercellular_mitochondri fill:#4fc3f7,stroke:#333,color:#000
    style Miro1_dysfunction fill:#4fc3f7,stroke:#333,color:#000
    style Parkinson_s_disease fill:#ef5350,stroke:#333,color:#000
    style Miro1_degradation fill:#4fc3f7,stroke:#333,color:#000
    style damaged_mitochondrial_spr fill:#4fc3f7,stroke:#333,color:#000
    style BNIP3_NIX fill:#4fc3f7,stroke:#333,color:#000
    style mitochondrial_turnover fill:#4fc3f7,stroke:#333,color:#000
    style BNIP3_NIX_inhibition fill:#4fc3f7,stroke:#333,color:#000
    style mitochondrial_transfer_ef fill:#4fc3f7,stroke:#333,color:#000
    style BNIP3_NIX_inhibition_1 fill:#4fc3f7,stroke:#333,color:#000
    style oxidative_stress fill:#4fc3f7,stroke:#333,color:#000
    style tunneling_nanotubes_2 fill:#4fc3f7,stroke:#333,color:#000
    style mitochondrial_transfer fill:#4fc3f7,stroke:#333,color:#000
    style F_actin fill:#4fc3f7,stroke:#333,color:#000
    style tunneling_nanotube_format fill:#4fc3f7,stroke:#333,color:#000
    style connexin_43_3 fill:#4fc3f7,stroke:#333,color:#000
    style astrocyte_to_neuron_mitoc fill:#4fc3f7,stroke:#333,color:#000
    style excessive_connexin_43_exp fill:#4fc3f7,stroke:#333,color:#000
    style cellular_toxicity fill:#4fc3f7,stroke:#333,color:#000

3D Protein Structure

🧬 RHOT1 — PDB 5KSZ Click to expand 3D viewer

Experimental structure from RCSB PDB | Powered by Mol* | Rotate: click+drag | Zoom: scroll | Reset: right-click

Source Analysis

Mitochondrial transfer between neurons and glia

neurodegeneration | 2026-04-01 | completed

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Same Analysis (5)

Astrocytic Connexin-43 Upregulation Enhances Neuroprotective Mitochond
Score: 0.56 · GJA1
PINK1/Parkin-Independent Mitophagy Bypass for Enhanced Donor Mitochond
Score: 0.53 · BNIP3/BNIP3L
Synthetic Biology Approach: Designer Mitochondrial Export Systems
Score: 0.51 · Synthetic fusion proteins
Microglia-Derived Extracellular Vesicle Engineering for Targeted Mitoc
Score: 0.48 · RAB27A/LAMP2B
Optogenetic Control of Mitochondrial Transfer Networks
Score: 0.48 · ChR2
→ View all analysis hypotheses
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