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The protein encoded by PTGER4 is a member of the G-protein coupled receptor family. De plus, nous expédions PTGER4 Anticorps (89) et beaucoup plus de produits pour cette protéine.
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Lkt/ABCC4 (Montrer ABCC4 Protéines)-mediated PGE2 signalling acts through a ciliary G-protein-coupled receptor (Montrer GPBAR1 Protéines), 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.
Case Report: elevated EP4 expression in pulmonary hypertension patient with dissecting pulmonary aneurysm.
Collectively, these results indicate that COX-1/PGE2/EP4 upregulates the beta-arr1 (Montrer ARRB1 Protéines) mediated Akt (Montrer AKT1 Protéines) 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 (Montrer S1PR3 Protéines) and its activation by S1P (Montrer MBTPS1 Protéines) has pro-inflammatory and pro-metastatic potential by inducing COX-2 expression and PGE2 signaling via EP2 (Montrer SPAG11B Protéines) 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 (Montrer MMRN1 Protéines), as well as the invasion of breast cancer cells in in vitro models.
EP4 expression can promote the development of resistance to aromatase (Montrer CYP19A1 Protéines) inhibitor therapy for breast cancer
Findings suggest SUMO-1 (Montrer SUMO1 Protéines) 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 (Montrer EGFR Protéines) interactive signaling.
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 (Montrer SPAG11A Protéines) receptors, and EPAC (Montrer RAPGEF3 Protéines) are prerequisites for maximal LPS (Montrer TLR4 Protéines)-induced IL-33 (Montrer IL33 Protéines) expression and that exogenous PGE2 can amplify IL-33 (Montrer IL33 Protéines) production via EP2 (Montrer SPAG11A Protéines) and EP4 receptors.
The data presented highlight a key role for EP2 (Montrer SPAG11A Protéines) and EP4 receptors in microvascular leak induced by PGE2.
These results suggest that Il23a (Montrer IL23A Protéines) expression in DCs is synergistically triggered by the PG E2-EP4-cAMP-PKA pathway and canonical/non-canonical NF-kappaB (Montrer NFKB1 Protéines) pathways and CREB (Montrer CREB1 Protéines) activated by CD40 (Montrer CD40 Protéines) stimulation.
autocrine prostaglandin E2 signaling through EP receptors is essential for optimal CD4 (Montrer CD4 Protéines)(+) T-cell activation.
Data suggest that lysophosphatidic acid (LPA (Montrer PLG Protéines)) up-regulates expression of SLCO2A1 (Montrer SLCO2A1 Protéines) (prostaglandin [PG] transporter), PTGER2 (Montrer PTGER2 Protéines)/PTGER4 (PG receptors EP2 (Montrer SPAG11A Protéines)/EP4), and mPGES1 (Montrer PTGES Protéines)/cPGES (Montrer PTGES3 Protéines) (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 (Montrer PTGER2 Protéines) (prostaglandin E receptor 2); EP4/PTGER4 (prostaglandin E receptor 4); and FP/PTGFR (prostaglandin F2alpha receptor (Montrer PTGFR Protéines)).
The PGE2-mediated down-regulation of CD25 (Montrer IL2RA Protéines) expression on T cells is mediated via the EP4 receptor, although selective activation of the EP2 receptor up-regulates the CD25 (Montrer IL2RA Protéines) expression on these cells.
EP4 is undetectable in endometrium and myometrium during the estrous cycle
Quantitative RT-PCR revealed significant higher expression of EP2 (Montrer SPAG11A Protéines) 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