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The protein encoded by PTGER4 is a member of the G-protein coupled receptor family. Additionally we are shipping PTGER4 Antibodies (89) and many more products for this protein.
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Lkt/ABCC4 (show ABCC4 Proteins)-mediated PGE2 signalling acts through a ciliary G-protein-coupled receptor (show GPBAR1 Proteins), EP4, to upregulate cAMP synthesis and increase anterograde intraflagellar transport, thereby promoting ciliogenesis.
Ep4a, a PGE2 receptor isoform of EP4, is involved in lymphoid precursor development in zebrafish.
Collectively, these results indicate that COX-1/PGE2/EP4 upregulates the beta-arr1 (show ARRB1 Proteins) mediated Akt (show AKT1 Proteins) signaling pathway to provide mucosal protection in colitis.
Reprogramming of mammary epithelial cells can result from EP4 -mediated stem cell property transfer by extracellular vesicles/exosomes containing caveolae-associated proteins, between mammary basal and luminal epithelial cells.
High PTGER4 methylation is associated with Lung cancer.
in breast cancer cells overexpression of S1P3 (show S1PR3 Proteins) and its activation by S1P (show MBTPS1 Proteins) has pro-inflammatory and pro-metastatic potential by inducing COX-2 expression and PGE2 signaling via EP2 (show SPAG11B Proteins) and EP4.
These results indicate that the blockage of PGE2-EP4 signaling prevents the bone destruction required for prostate cancer metastases, and that this is, in part due to the abrogation of bone cell responses. The study provides further evidence that an EP4 antagonist is a candidate for the treatment of prostate cancer in the blockade of bone metastasis.
The results show that stimulation with the selective EP4 agonist CAY10598 or PGE2 promotes invadopodia-mediated degradation of the ECM (show MMRN1 Proteins), as well as the invasion of breast cancer cells in in vitro models.
EP4 expression can promote the development of resistance to aromatase (show CYP19A1 Proteins) inhibitor therapy for breast cancer
Findings suggest SUMO-1 (show SUMO1 Proteins) protein and PGE2 receptor subtype 4 (EP4) as two potential targets for new therapeutic or prevention strategies for endometrial cancers.
GW627368X therefore effectively inhibits cervical cancer survival, motility, proliferation and angiogenesis by blocking EP4/EGFR (show EGFR Proteins) interactive signaling.
The cross-talk between SP1 (show PSG1 Proteins) and p65 (show GORASP1 Proteins), and the positive feedback regulatory loop of PI3-K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling by EP4 contribute to the overall responses of solamargine in this process
Paricalcitol also attenuated the infiltration of inflammatory cells and production of proinflammatory cytokines after IR injury. EP4 antagonist abolished these antioxidant, anti-inflammatory, and antiapoptotic effects. The EP4 plays a pivotal role in the protective effects of paricalcitol in renal IR injury.
These results demonstrate a novel role for prostaglandin receptor EP4 in the mediation of barrier-enhancing and anti-inflammatory effects caused by oxidized phospholipids.
The deletion of EP4 increases mitochondrial biogenesis and oxidative capacity in WAT, and fat mass loss ensues in mice.
Myeloid cell Ptger4 modulates interleukin production but not atherogenesis in type I diabetic mice.
These data suggest that vascular EP4 receptors buffer the actions of AngII on renal hemodynamics and oxidative injury.
these studies have demonstrated an important but unexpected role for macrophage COX-2/prostaglandin E2/PGE2 receptor subtype 4 signaling to lessen progression of diabetic kidney disease, unlike the pathogenic effects of increased COX-2 expression in intrinsic renal cells.
data demonstrate that endogenous PGE2, EP2 (show SPAG11A Proteins) receptors, and EPAC (show RAPGEF3 Proteins) are prerequisites for maximal LPS (show TLR4 Proteins)-induced IL-33 (show IL33 Proteins) expression and that exogenous PGE2 can amplify IL-33 (show IL33 Proteins) production via EP2 (show SPAG11A Proteins) and EP4 receptors.
The data presented highlight a key role for EP2 (show SPAG11A Proteins) and EP4 receptors in microvascular leak induced by PGE2.
These results suggest that Il23a (show IL23A Proteins) expression in DCs is synergistically triggered by the PG E2-EP4-cAMP-PKA pathway and canonical/non-canonical NF-kappaB (show NFKB1 Proteins) pathways and CREB (show CREB1 Proteins) activated by CD40 (show CD40 Proteins) stimulation.
autocrine prostaglandin E2 signaling through EP receptors is essential for optimal CD4 (show CD4 Proteins)(+) T-cell activation.
Data suggest that lysophosphatidic acid (LPA (show PLG Proteins)) up-regulates expression of SLCO2A1 (show SLCO2A1 Proteins) (prostaglandin [PG] transporter), PTGER2 (show PTGER2 Proteins)/PTGER4 (PG receptors EP2 (show SPAG11A Proteins)/EP4), and mPGES1 (show PTGES Proteins)/cPGES (show PTGES3 Proteins) (microsomal/cytosolic PG E synthases) in luteal cells.
Data suggest that estradiol up-regulates mRNA and protein expression of 3 prostanoid receptors in oviduct smooth muscle: EP2/PTGER2 (show PTGER2 Proteins) (prostaglandin E receptor 2); EP4/PTGER4 (prostaglandin E receptor 4); and FP/PTGFR (prostaglandin F2alpha receptor (show PTGFR Proteins)).
The PGE2-mediated down-regulation of CD25 (show IL2RA Proteins) expression on T cells is mediated via the EP4 receptor, although selective activation of the EP2 receptor up-regulates the CD25 (show IL2RA Proteins) expression on these cells.
EP4 is undetectable in endometrium and myometrium during the estrous cycle
Quantitative RT-PCR revealed significant higher expression of EP2 (show SPAG11A Proteins) and EP4 in the pre-ovulatory phase compared with the luteal phase in the bovine oviduct
The protein encoded by this gene is a member of the G-protein coupled receptor family. This protein is one of four receptors identified for prostaglandin E2 (PGE2). This receptor can activate T-cell factor signaling. It has been shown to mediate PGE2 induced expression of early growth response 1 (EGR1), regulate the level and stability of cyclooxygenase-2 mRNA, and lead to the phosphorylation of glycogen synthase kinase-3. Knockout studies in mice suggest that this receptor may be involved in the neonatal adaptation of circulatory system, osteoporosis, as well as initiation of skin immune responses.
prostaglandin E receptor 4, subtype EP4
, prostaglandin E2 receptor EP4 subtype
, prostaglandin E2 receptor subtype 4
, prostaglandin E receptor 4 (subtype EP4)
, prostaglandin E receptor 4
, prostaglandin E receptor 4 subtype EP4
, PGE receptor EP4 subtype
, PGE receptor, EP4 subtype
, PGE2 receptor EP4 subtype
, prostanoid EP4 receptor
, prostaglandin E receptor 4 (EP4 subtype)
, prostaglandin E receptor EP4 subtype
, prostaglandin E2 receptor type 4
, PGE receptor, subtype EP4
, prostaglandin receptor EP4 subtype
, prostaglandin E2 subtype EP4 receptor