🧪
hypothesis

RAB29 Is the Critical Molecular Switch That Determines Whether LRRK2 Signal Amplification Occurs (H4)

Hypothesis

RAB29 Is the Critical Molecular Switch That Determines Whether LRRK2 Signal Amplification Occurs (H4)

RAB29 functions as a gatekeeper—when lysosomes swell, RAB29-GTP increases, recruits LRRK2, and G2019S hyperphosphorylates RAB10 disproportionately.
🧬 RAB29🩺 neurodegeneration🎯 Composite 71%💱 $0.57▼13.2%proposed
EvidencePending (0%)📖 8 cit🗣 1 debates 8 support 2 oppose
✓ All Quality Gates Passed
Mechanistic 0.72 (15%) Evidence 0.70 (15%) Novelty 0.82 (12%) Feasibility 0.78 (12%) Impact 0.80 (12%) Druggability 0.52 (10%) Safety 0.78 (8%) Competition 0.72 (6%) Data Avail. 0.62 (5%) Reproducible 0.68 (5%) KG Connect 0.50 (8%) 0.710 composite
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Composite71%

🧪 Overview

RAB29 functions as a gatekeeper—when lysosomes swell, RAB29-GTP increases, recruits LRRK2, and G2019S hyperphosphorylates RAB10 disproportionately. The amplification is RAB29-dependent. Strategic pivot: RAB29 serves as predictive biomarker rather than drug target. RAB29 knockout in G2019S patient-derived neurons would determine if amplification requires RAB29.

🧬 Mechanism

🧬 Curated Mechanism Pathway

Curated pathway from expert analysis

flowchart TD
    A["RAB29 GTPase<br/>Activity"]
    B["Recruitment to<br/>Stressed Lysosomes"]
    C["Enhanced LRRK2-mediated<br/>Rab Phosphorylation"]
    D["Lysosomal<br/>Dysfunction"]
    E["Autophagy<br/>Impairment"]
    F["Neuronal<br/>Death"]
    G["Modifier of LRRK2<br/>Pathogenesis"]
    A --> B
    B --> C
    C --> D
    D --> E
    E --> F
    A --> G
    G --> C
    style A fill:#1a237e,stroke:#4fc3f7,color:#4fc3f7
    style F fill:#b71c1c,stroke:#ef9a9a,color:#ef9a9a
    style G fill:#1b5e20,stroke:#a5d6a7,color:#a5d6a7

⚖️ Evidence

⚖️ Evidence Matrix8 supports2 contradicts
Supports
RAB29 localizes to swollen lysosomes
PMID:30635564
Supports
RAB29 activates LRRK2 in cells
PMID:28067317
Supports
RAB29 knockout rescues LRRK2 pathogenic phenotypes in zebrafish
PMID:31743699
Supports
Endogenous Rab29 does not impact basal or stimulated LRRK2 pathway activity.
Biochem J2020PMID:33135724medium
Supports
LRRK2 and Parkinson's disease: from genetics to targeted therapy.
Ann Clin Transl Neurol2023PMID:37021623medium
Supports
LRRK2 in Parkinson's disease: upstream regulation and therapeutic targeting.
Trends Mol Med2024PMID:39153957medium
Supports
LRRK2 mediates tubulation and vesicle sorting from lysosomes.
Sci Adv2020PMID:33177079medium
Supports
The Cell Biology of LRRK2 in Parkinson's Disease.
Mol Cell Biol2021PMID:33526455medium
Contradicts
Zebrafish data may not translate to mammalian neurons
PMID:31743699
Contradicts
RAB29 mutations cause disease through LRRK2 activation—switch model unclear
PMID:28165311
📖 Linked Papers

No linked papers recorded for this hypothesis yet.

🏥 Translation

🧬 3D Protein Structure — RAB29

No curated PDB or AlphaFold mapping for RAB29 yet. Search RCSB →

🧠 GTEx v10 Brain ExpressionJSON

Median TPM across 13 brain regions for RAB29 from GTEx v10.

Spinal cord cervical c-113.6 Substantia nigra13.2 Caudate basal ganglia11.8 Cortex10.8 Frontal Cortex BA910.7 Anterior cingulate cortex BA2410.6 Amygdala10.1 Hypothalamus9.9 Putamen basal ganglia9.9 Nucleus accumbens basal ganglia9.8 Cerebellum9.3 Hippocampus8.1 Cerebellar Hemisphere7.5median TPM (GTEx v10)

💉 Clinical Trials

No clinical trials data linked to this hypothesis yet.

No curated ClinVar variants loaded for this hypothesis.

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

🔍 Search ClinVar for RAB29 →

No DepMap CRISPR Chronos data found for RAB29.

Run python3 scripts/backfill_hypothesis_depmap.py to populate.

🏆 Tournament

🏆 Arenas / Elo

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📊 Market Indicators

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💾 Resource Usage

No resource usage or linked notebooks recorded for this hypothesis yet.

🔮 Predictions

🔎 Predictions vs Observations2 predictions · 0 with recorded observations
PredictionPredictedObservedStatusConf
IF CRISPR-Cas9-mediated RAB29 knockout is performed in G2019S patient-derived iPSC neurons, THEN RAB10 phosphorylation at Thr73 will be reduced by at least 50% compared to isogenic G2019S control neurAt least 50% reduction in phospho-RAB10 (Thr73) levels in RAB29 knockout G2019S neurons relative to G2019S parental neurons, as measured by multiplex immunoassa— no observation —pending0.72
IF RAB29 is overexpressed via AAV-mediated transduction in non-swollen lysosomes of G2019S patient-derived neurons, THEN LRRK2-mediated RAB10 phosphorylation will not increase above baseline, whereas AAV-RAB29 overexpression alone will not elevate phospho-RAB10; however, pretreatment with hypotonic medium (5-10 min) to induce lysosome swelling will produce s— no observation —pending0.68
🔮 Falsifiable Predictions (2)
pendingconf 72%
IF CRISPR-Cas9-mediated RAB29 knockout is performed in G2019S patient-derived iPSC neurons, THEN RAB10 phosphorylation at Thr73 will be reduced by at least 50% compared to isogenic G2019S control neurons within 6 weeks of neuronal differentiation.
Predicted outcome: At least 50% reduction in phospho-RAB10 (Thr73) levels in RAB29 knockout G2019S neurons relative to G2019S parental neurons, as measured by multiplex
Falsification: No significant change (<20%) in phospho-RAB10 (Thr73) levels between RAB29 knockout and parental G2019S neurons, indicating LRRK2 G2019S can hyperphosphorylate RAB10 independently of RAB29
pendingconf 68%
IF RAB29 is overexpressed via AAV-mediated transduction in non-swollen lysosomes of G2019S patient-derived neurons, THEN LRRK2-mediated RAB10 phosphorylation will not increase above baseline, whereas osmotic lysosome swelling will rescue hyperphosphorylation in a RAB29-dependent manner within 3 week
Predicted outcome: AAV-RAB29 overexpression alone will not elevate phospho-RAB10; however, pretreatment with hypotonic medium (5-10 min) to induce lysosome swelling will
Falsification: RAB29 overexpression alone significantly increases (>30%) phospho-RAB10 levels without lysosome swelling, contradicting the gatekeeper model, OR RAB29 knockout neurons retain normal RAB10 hyperphospho
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