Application | Comment | Organism |
---|---|---|
drug development | inhibition of iPLA2 and lysophospholipid production may be of interest to reduce Ca2+ entry and subsequent degeneration of dystrophic muscle | Mus musculus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
AACOCF3 | PLA2 inhibitor, does not affect basal Mn2+ entry, but strongly reduces the enhanced Mn2+ entry of thapsigargin-treated fibers | Mus musculus | |
bromoenol lactone | specific suicide substrate of PLA2, does not affect basal Mn2+ entry, but strongly reduces the enhanced Mn2+ entry of thapsigargin-treated fibers | Mus musculus |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
additional information | iPLA2 is primarily located in the vicinity of the sarcolemma | Mus musculus | - |
- |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
muscle | murine model of Duchenne muscular dystrophy | Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | production of lysophosphatidylcholine | Mus musculus | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
Ca2+-independent PLA2 | - |
Mus musculus |
iPLA2 | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
physiological function | iPLA2 is responsible for the enhanced Mn2+ entry occurring upon Ca2+ store depletion, iPLA2 hydrolysis products are involved in the gating of store-operated channels | Mus musculus |