Entity Detail — Knowledge Graph Node
This page aggregates everything SciDEX knows about ATP13A3: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.
ATP13A3 encodes a P5-type ATPase (ATP13A3/P5-ATPase) that functions as a cation transporter with specificity for calcium and other divalent cations. ATP13A3 is closely related to ATP13A2 (PARK9), and variants are associated with Parkinson's disease and pulmonary hypertension.
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| Gene Symbol | ATP13A3 |
| Full Name | ATPase 13A3 (P5-ATPase) |
| Aliases | ATP13A3/P5-ATPase |
| Chromosome | 3q29 |
| Function | encodes a P5-type P-type ATPase (P5-ATPase) that functions as a cation transporter with specificity for calcium and other divalent cations. |
| Subcellular Localization | Non-redundant in some contexts |
| Molecular Weight | 120 kDa |
| Amino Acids | 1058 aa |
| Exons | 25 |
| UniProt ID | Q9HAW4 |
| NCBI Gene ID | 79572 |
| Ensembl ID | ENSG00000165621 |
| OMIM | 615044 |
| GeneCards | ATP13A3 |
| Human Protein Atlas | ATP13A3 |
| Associated Diseases | Parkinson's disease |
| Databases | GeneCardsHPASTRING |
Knowledge base pages for this entity
graph TD
ATP13A3["ATP13A3
(P5-type ATPase)"]
ATP13A3 -->|"transports"| polyamines["Polyamine Transport
(spermidine, spermine)"]
ATP13A3 -->|"maintains"| lysosomal_pH["Lysosomal pH
Homeostasis"]
ATP13A3 -->|"regulates"| autophagy["Autophagy
Process"]
polyamines -->|"supports"| protein_folding["Protein Folding
Quality Control"]
polyamines -->|"protects"| mitochondria["Mitochondrial
Function"]
lysosomal_pH -->|"enables"| enzyme_activity["Lysosomal Enzyme
Activity"]
lysosomal_pH -->|"facilitates"| protein_degradation["Protein
Degradation"]
autophagy -->|"clears"| misfolded_proteins["Misfolded Protein
Clearance"]
autophagy -->|"removes"| damaged_organelles["Damaged Organelle
Removal"]
ATP13A3_dysfunction["ATP13A3
Dysfunction"] -->|"impairs"| ATP13A3
ATP13A3_dysfunction -->|"leads to"| lysosomal_dysfunction["Lysosomal
Dysfunction"]
ATP13A3_dysfunction -->|"causes"| polyamine_imbalance["Polyamine
Imbalance"]
lysosomal_dysfunction -->|"contributes to"| neurodegeneration["Neurodegeneration"]
polyamine_imbalance -->|"promotes"| oxidative_stress["Oxidative
Stress"]
oxidative_stress -->|"accelerates"| neurodegeneration
misfolded_proteins -->|"accumulate in"| neurodegeneration
classDef central fill:#1a3a4a,stroke:#4fc3f7,stroke-width:3px,color:#ffffff
classDef protective fill:#1a3a2a,stroke:#81c784,stroke-width:2px,color:#ffffff
classDef pathological fill:#3a1a1a,stroke:#ef5350,stroke-width:2px,color:#ffffff
classDef regulatory fill:#2a1a3a,stroke:#ce93d8,stroke-width:2px,color:#ffffff
classDef disease fill:#3a2a1a,stroke:#ffa726,stroke-width:2px,color:#ffffff
class ATP13A3 central
class polyamines,protein_folding,mitochondria,enzyme_activity,protein_degradation,autophagy,misfolded_proteins,damaged_organelles protective
class ATP13A3_dysfunction,lysosomal_dysfunction,polyamine_imbalance,oxidative_stress pathological
class lysosomal_pH regulatory
class neurodegeneration disease| Target | Relation | Type | Str |
|---|---|---|---|
| No outgoing edges | |||
| Source | Relation | Type | Str |
|---|---|---|---|
| No incoming edges | |||
Hypotheses where this entity is a therapeutic target
| Hypothesis | Score | Disease | Analysis |
|---|---|---|---|
| No targeting hypotheses | |||
Scientific analyses that reference this entity
No analyses mention this entity
Experimental studies targeting or related to this entity
| Experiment | Type | Disease | Score | Feasibility | Model | Status | Est. Cost |
|---|---|---|---|---|---|---|---|
| No experiments found | |||||||
Scientific publications cited in analyses involving this entity
| Title & PMID | Authors | Journal | Year | Citations |
|---|---|---|---|---|
| No papers found | ||||
Multi-agent debates referencing this entity
No debates reference this entity
Hypotheses and analyses mentioning ATP13A3 in their description or question text
No additional research found