🧫
cGAS/STING pathway validation in TDP-43 mutant mice
active
experiment
Created: 2026-04-06T12:28:40
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-9611670e-a7a5-48cc-a6cc-6d2aa0ddce50
🧫 Experiment Protocol
ValidationAmyotrophic Lateral SclerosisTARDBPTDP-43 mutant miceproposed
Validation study using TDP-43 mutant mice to confirm the role of cGAS/STING signaling in TDP-43-associated neuroinflammation. The experiment involved pharmacologic inhibition or genetic deletion of cGAS and STING components to assess their impact on NF-κB and type I interferon upregulation induced by TDP-43 mutations. This in vivo model provided crucial evidence that the cGAS/STING pathway is a key mediator of TDP-43-driven neuroinflammation in the context of a whole organism with intact immune and nervous systems.
PRIMARY OUTCOME
Prevention of NF-κB and type I IFN upregulation
EXPECTED OUTCOMES
cGAS/STING inhibition should prevent TDP-43-induced neuroinflammatory responses and potentially ameliorate disease progression
SUCCESS CRITERIA
Significant reduction in inflammatory markers and improved neurological outcomes with cGAS/STING pathway inhibition
PROTOCOL
TDP-43 mutant mouse generation, cGAS/STING inhibition via pharmacologic or genetic approaches, inflammatory marker analysis, behavioral and pathological assessments
LINKED HYPOTHESES
Source: PMID 33031745 ↗
🧫 Experiment Extras
PATHWAY
cGAS/STING, NF-κB, type I interferon pathways
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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