Prostaglandin E2 - CAS 363-24-6
Catalog number: 363-24-6
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Prostanoid Receptor
Binds with high affinity to EP1, EP2, EP3 and EP4 receptors (Kd values range between ~ 1 - 10 nM), Prostaglandin E2 is one of the primary COX products of arachidonic acid and one of the most widely investigated prostaglandins.
White solid
PGE2; PGE 2; PGE-2; U 12062; U12062; U-12062; Dinoprostone; Prostenone; Prostin(Z)-7-[(1R,2R,3R)-3-hydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]-5-oxocyclopentyl]hept-5-enoic acid
Soluble in DMSO
Store at -20 °C
Endogenous prostaglandin and primary product of arachidonic acid/cyclooxygenase pathway.
Quality Standard:
Enterprise standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly.
Boiling Point:
530.071ºC at 760 mmHg
Melting Point:
1.148 g/cm3
Canonical SMILES:
1.Role of prostaglandin E2 in the modulation of Wnt canonical signaling in cells on microstructured titanium surfaces.
Manfredi E1,2, Lumetti S1,2, Rivara F2, Toffoli A1,2, Calciolari E1, Cacchioli A3, Ravanetti F3, Ghiacci G1, Macaluso G1,2,4, Galli C1,2,4. J Appl Biomater Funct Mater. 2016 May 6:0. doi: 10.5301/jabfm.5000267. [Epub ahead of print]
BACKGROUND: Rough surface topography enhances the activation of Wnt canonical signaling, a pathway required for osteoblast differentiation. The present study investigated the effects of the modulation of prostaglandin E2 (PGE2) signaling on osteoblastic differentiation on titanium surfaces for endosseous implants with different topographies.
2.Prostaglandin E2-Dependent Phosphorylation of RAS Inhibition 1 (RIN1) at Ser 291 and 292 Inhibits Transforming Growth Factor-β-Induced RAS Activation Pathway in Human Synovial Fibroblasts: Role in Cell Migration.
Gerarduzzi C1, He Q2, Zhai B2, Antoniou J3, Di Battista JA2. J Cell Physiol. 2016 May 2. doi: 10.1002/jcp.25412. [Epub ahead of print]
Prostaglandin E2 (PGE2 )-stimulated G-protein coupled receptor (GPCR) activation inhibits pro-fibrotic TGFβ-dependent stimulation of human fibroblast to myofibroblast transition (FMT), though the precise molecular mechanisms are not fully understood. In the present study, we describe the PGE2 -dependent suppression and reversal of TGFβ-induced events such as α-sma expression, stress fiber formation, and Ras/Raf/ERK/MAPK pathway-dependent activation of myofibroblast migration. In order to elucidate post ligand-receptor signaling pathways, we identified a predominant PKA phosphorylation motif profile in human primary fibroblasts after treatment with exogenous PGE2 (EC50 30nM, Vmax 100nM), mimicked by the adenyl cyclase activator forskolin (EC50 5µM, Vmax 10µM). We used a global phosphoproteomic approach to identify a 2.5 fold difference in PGE2 induced phosphorylation of proteins containing the PKA motif. Deducing the signaling pathway of our migration data, we identified Ras inhibitor 1 (RIN1) as a substrate, whereby PGE2 induced its phosphorylation at Ser291 and at Ser292 by a 5.
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CAS 363-24-6 Prostaglandin E2

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