🧫
PTEC-specific RUBCN knockout mice phenotyping
active
experiment
Created: 2026-04-06T12:33:52
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-c94e78e4-305e-43b6-843d-248bd374ee01
🧫 Experiment Protocol
Validationacute kidney injury and metabolic syndromeRUBCNPTEC-specific RUBCN knockout miceproposed
Generated proximal tubular epithelial cell (PTEC)-specific RUBCN-deficient knockout mice to investigate the physiological role of RUBCN in kidney cells. Analyzed the phenotype including autophagy flux, kidney injury protection, and metabolic parameters. Found that despite sustained high autophagic flux in PTECs, KO mice were not protected from acute ischemic kidney injury. Unexpectedly, KO mice developed features of metabolic syndrome with expanded lysosomes containing multi-layered phospholipids in PTECs.
PRIMARY OUTCOME
autophagy flux and metabolic syndrome development
EXPECTED OUTCOMES
Expected protection from kidney injury due to enhanced autophagy
SUCCESS CRITERIA
Measurement of autophagic flux markers, kidney injury parameters, and metabolic syndrome features
PROTOCOL
Generated conditional knockout mice with PTEC-specific RUBCN deletion, performed ischemia-reperfusion injury models, analyzed metabolic parameters and lysosomal morphology
Source: PMID 31944172 ↗
🧫 Experiment Extras
PATHWAY
autophagy-lysosomal pathway
MARKET PRICE
$0.50
STATUS
proposed
▸Metadataorigin_type: v1_polymorphic_backfill
| origin_type | v1_polymorphic_backfill |
| source_table | experiments |
| _schema_version | 1 |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
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