🧫
GPR109A receptor validation using knockout macrophages
active
experiment
Created: 2026-04-10T22:50:14
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-2958fb94-6ae5-4fc8-a45f-26c1e015282e
🧫 Experiment Protocol
ExploratoryMycoplasma pneumoniae pneumoniaGPR109A, MAPK1, MAPK14, MAPK8, MAPK9GPR109A knockout mouse macrophagesproposed
GPR109A knockout mouse macrophages were used to confirm that the G-protein coupled receptor GPR109A mediates butyric acid's action in QTJD's therapeutic mechanism. This experiment was designed to validate the butyrate-GPR109A-MAPK pathway hypothesis. In GPR109A-/- macrophages, QTJD treatment still suppressed p38 and JNK1/2 MAPK proteins but showed no effect on ERK1/2, providing evidence that ERK1/2 inhibition by QTJD specifically requires GPR109A receptor signaling, while p38 and JNK1/2 inhibition may involve additional GPR109A-independent mechanisms. This experiment confirmed the involvement of the butyrate-GPR109A-MAPK pathway in QTJD's anti-inflammatory effects.
PRIMARY OUTCOME
Differential MAPK pathway responses in GPR109A-/- cells
EXPECTED OUTCOMES
GPR109A-dependent effects on ERK1/2 but not p38/JNK1/2
SUCCESS CRITERIA
Selective loss of ERK1/2 inhibition in GPR109A-/- cells
PROTOCOL
Western blotting analysis of MAPK proteins in GPR109A knockout macrophages treated with QTJD
Source: PMID 41754753 ↗
🧫 Experiment Extras
PATHWAY
Butyrate-GPR109A-MAPK signaling 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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