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Literature summary for 3.1.1.4 extracted from

  • Boittin, F.X.; Shapovalov, G.; Hirn, C.; Ruegg, U.T.
    Phospholipase A2-derived lysophosphatidylcholine triggers Ca2+ entry in dystrophic skeletal muscle fibers (2010), Biochem. Biophys. Res. Commun., 391, 401-406.
    View publication on PubMed

Application

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

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

Localization Comment Organism GeneOntology No. Textmining
additional information iPLA2 is primarily located in the vicinity of the sarcolemma Mus musculus
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-

Organism

Organism UniProt Comment Textmining
Mus musculus
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-
-

Source Tissue

Source Tissue Comment Organism Textmining
muscle murine model of Duchenne muscular dystrophy Mus musculus
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information production of lysophosphatidylcholine Mus musculus ?
-
?

Synonyms

Synonyms Comment Organism
Ca2+-independent PLA2
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Mus musculus
iPLA2
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Mus musculus

General Information

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