Entity Detail — Knowledge Graph Node
This page aggregates everything SciDEX knows about LYSOSOMAL ACIDIFICATION: 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.
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| Name | LYSOSOMAL ACIDIFICATION |
| Key Genes/Proteins | APP-ΒCTF |
graph TD
LYSOSOMAL_ACIDIFICATION[LYSOSOMAL ACIDIFICATION]
LYSOSOMAL_ACIDIFICATION -->|promotes| Hydrolase_Activity[Hydrolase Activity]
LYSOSOMAL_ACIDIFICATION -->|involved_in| AUTOPHAGY[AUTOPHAGY]
LYSOSOMAL_ACIDIFICATION -->|regulates| alpha_synuclein[alpha-synuclein]
Palmitate[Palmitate] -->|inhibits| LYSOSOMAL_ACIDIFICATION
AMPK[AMPK] -.protects against.-> LYSOSOMAL_ACIDIFICATION
LAMP1[LAMP1] -->|promotes| LYSOSOMAL_ACIDIFICATION
LAMP2[LAMP2] -->|promotes| LYSOSOMAL_ACIDIFICATION
C19ORF12[C19ORF12] -->|regulates| LYSOSOMAL_ACIDIFICATION
APP__CTF[APP-ΒCTF] -->|inhibits| LYSOSOMAL_ACIDIFICATION
ATP6AP2[ATP6AP2] -->|participates in| LYSOSOMAL_ACIDIFICATION
ATP6V1G1[ATP6V1G1] -->|regulates| LYSOSOMAL_ACIDIFICATION| Target | Relation | Type | Str |
|---|---|---|---|
| lysosomal hydrolytic function | associated_with | process | 0.90 |
| PROTEIN_DEGRADATION | associated_with | pathway | 0.90 |
| Hydrolase Activity | promotes | process | 0.85 |
| AUTOPHAGY | involved_in | process | 0.85 |
| TFEB activation | regulates | phenotype | 0.70 |
| alpha-synuclein | regulates | protein | 0.70 |
| protein degradation | enables | process | 0.70 |
| seed_degradation | associated_with | phenotype | 0.70 |
| Autophagy Flux | regulates | phenotype | 0.70 |
| Source | Relation | Type | Str |
|---|---|---|---|
| Palmitate | inhibits | compound | 0.95 |
| AMPK | protects_against | protein | 0.95 |
| LAMP1 | associated_with | protein | 0.90 |
| LAMP2 | associated_with | protein | 0.90 |
| Aβ42 | impairs | protein | 0.90 |
| neuronal lysosomes | regulates | cell_type | 0.90 |
| ATP6V1A | encodes_subunit_of | gene | 0.90 |
| APP-ΒCTF | inhibits | protein | 0.80 |
| C19ORF12 | regulates | gene | 0.80 |
| ATP6AP2 | participates_in | gene | 0.80 |
| LAMP1 | regulates | protein | 0.70 |
| OXPHOS failure | causes | process | 0.70 |
| OXPHOS failure | inhibits | process | 0.70 |
| V-ATPase assembly | regulates | phenotype | 0.70 |
| ATP6V1A | regulates | gene | 0.70 |
| ATP6V1G1 | regulates | gene | 0.70 |
| TFEB | regulates | gene | 0.70 |
Hypotheses where this entity is a therapeutic target
| Hypothesis | Score | Disease | Analysis |
|---|---|---|---|
| Compromised Lysosomal Acidification and Trafficking Due to N | 0.718 | neurodegeneration | What mechanisms underlie neuronal resist |
| Lysosomal Acidification Failure: Convergent GBA1/LAMP2A–medi | 0.700 | neurodegeneration | - |
| Restoration of V-ATPase function reverses lysosomal acidific | 0.630 | neuroscience | Lysosomal dysfunction and cathepsin leak |
Scientific analyses that reference this entity
neurodegeneration | 2026-04-26 | 0 hypotheses
neurodegeneration | 2026-04-16 | 2 hypotheses Top: 0.575
neurodegeneration | 2026-04-08 | 7 hypotheses Top: 0.455
neurodegeneration | 2026-04-07 | 5 hypotheses Top: 0.718
neuroscience | 2026-04-04 | 7 hypotheses Top: 0.679
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
closed · Rounds: 6 · Score: 0.50 · 2026-04-25
closed · Rounds: 4 · Score: 0.76 · 2026-04-22
closed · Rounds: 4 · Score: 0.65 · 2026-04-21
closed · Rounds: 4 · Score: 0.72 · 2026-04-21
closed · Rounds: 4 · Score: 0.46 · 2026-04-16
closed · Rounds: 4 · Score: 0.95 · 2026-04-10
closed · Rounds: 4 · Score: 0.95 · 2026-04-03
Hypotheses and analyses mentioning LYSOSOMAL ACIDIFICATION in their description or question text
No additional research found