Prostaglandin E Receptor 4 (Subtype EP4) Proteins (PTGER4)

Zebrafish Prostaglandin E Receptor 4 (Subtype EP4) (PTGER4) interaction partners

1. Lkt/ABCC4-mediated PGE2 signalling acts through a ciliary G-protein-coupled receptor, EP4, to upregulate cAMP synthesis and increase anterograde intraflagellar transport, thereby promoting ciliogenesis.

2. Ep4a, a PGE2 receptor isoform of EP4, is involved in lymphoid precursor development in zebrafish.

Human Prostaglandin E Receptor 4 (Subtype EP4) (PTGER4) interaction partners

1. discovery of recurrent PTGER4 amplification implies a potential of exploring targeting therapy to the prostaglandin synthesis pathways in a subset of these tumors

2. High EP4 expression is associated with chemoresistant breast carcinoma.

3. Study demonstrated that the expression of EP4 receptors was up-regulated by c-Myc by binding to Sp-1 under low cellular density conditions but was down-regulated under high cellular density conditions via the increase in the expression levels of HIF-1alpha protein, which may pull out c-Myc and Sp-1 from DNA-binding.

4. results indicate that PGE2 inhibits hCAP18/LL-37 expression, especially VD3-induced cathelicidin and autophagy, which may reduce host defense against Mtb. Accordingly, antagonists of EP4 may constitute a novel adjunctive therapy in Mtb infection.

5. Case Report: elevated EP4 expression in pulmonary hypertension patient with dissecting pulmonary aneurysm.

6. Collectively, these results indicate that COX-1/PGE2/EP4 upregulates the beta-arr1 mediated Akt signaling pathway to provide mucosal protection in colitis.

7. 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.

8. High PTGER4 methylation is associated with Lung cancer.

9. in breast cancer cells overexpression of S1P3 and its activation by S1P has pro-inflammatory and pro-metastatic potential by inducing COX-2 expression and PGE2 signaling via EP2 and EP4.

10. 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.

11. The results show that stimulation with the selective EP4 agonist CAY10598 or PGE2 promotes invadopodia-mediated degradation of the ECM, as well as the invasion of breast cancer cells in in vitro models.

12. EP4 expression can promote the development of resistance to aromatase inhibitor therapy for breast cancer

13. Findings suggest SUMO-1 protein and PGE2 receptor subtype 4 (EP4) as two potential targets for new therapeutic or prevention strategies for endometrial cancers.

14. GW627368X therefore effectively inhibits cervical cancer survival, motility, proliferation and angiogenesis by blocking EP4/EGFR interactive signaling.

15. The cross-talk between SP1 and p65, and the positive feedback regulatory loop of PI3-K/Akt signaling by EP4 contribute to the overall responses of solamargine in this process

16. The PTGER4 gene is a candidate risk factor for radiological progression in rheumatoid arthritis

17. IP and EP4 receptors have a role in prostanoid regulation of angiogeneis

18. miRNA 526b is a COX-2 upregulated, oncogenic miRNA promoting stem-like cells, the expression of which follows EP4 receptor-mediated signaling.

19. Altered inhibitory function of the EP4R in eosinophils and monocytes from aspirin-intolerant patients

20. data show a protective role for the PGE2 receptors EP(2) and EP(4) following osmotic changes, through the reduction of human mast cell activity caused by calcium influx impairment and MAP kinase inhibition.

Mouse (Murine) Prostaglandin E Receptor 4 (Subtype EP4) (PTGER4) interaction partners

1. Our data suggest that deletion of EP4 in S100a4-lineage cells inhibits range of motion-limiting scar tissue without further compromising mechanical properties.

2. EP4 enhancement aggravated imbalanced mesangial cell proliferation stimulated by TGFbeta1 and GS of mice treated with 5/6 nephrectomy through the Smad and mitogenactivated protein kinase pathways.

3. EP4 is a novel regulator of bile acid synthesis, and its activation protects against hypercholesterolemia.

4. 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.

5. These results demonstrate a novel role for prostaglandin receptor EP4 in the mediation of barrier-enhancing and anti-inflammatory effects caused by oxidized phospholipids.

6. The deletion of EP4 increases mitochondrial biogenesis and oxidative capacity in WAT, and fat mass loss ensues in mice.

7. Myeloid cell Ptger4 modulates interleukin production but not atherogenesis in type I diabetic mice.

8. These data suggest that vascular EP4 receptors buffer the actions of AngII on renal hemodynamics and oxidative injury.

9. the roles of prostaglandin E2 (PGE2) receptor (EP) signaling in enhancement of lymphangiogenesis in wound healing processes

10. 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.

11. data demonstrate that endogenous PGE2, EP2 receptors, and EPAC are prerequisites for maximal LPS-induced IL-33 expression and that exogenous PGE2 can amplify IL-33 production via EP2 and EP4 receptors.

12. The data presented highlight a key role for EP2 and EP4 receptors in microvascular leak induced by PGE2.

13. It mediates neuritogenesis in sensory neuron.

14. These results suggest that Il23a expression in DCs is synergistically triggered by the PG E2-EP4-cAMP-PKA pathway and canonical/non-canonical NF-kappaB pathways and CREB activated by CD40 stimulation.

15. autocrine prostaglandin E2 signaling through EP receptors is essential for optimal CD4(+) T-cell activation.

16. PGE2-mediated EP4 signaling in myeloid cells promotes tumorigenesis.

17. the blockade of EP2 and EP4 promotes mouse survival after cryptococcus infection by promoting the production of cytokines via TLR4, as well as the enhanced M1 polarization of alveolar macrophages

18. the lean phenotype of EP4-deficient mice resulted from reduction in adipose tissue and accretion of other peripheral organs caused by impaired triglyceride clearance

19. These findings suggest that systemic EP4 antagonism leads to increased adhesion formation and matrix deposition during flexor tendon healing.

20. These data suggest that EPRAP in macrophages functions crucially in suppressing colonic inflammation. Consistently, EPRAP-positive macrophages were also accumulated in the colonic stroma of ulcerative colitis patients.

Cow (Bovine) Prostaglandin E Receptor 4 (Subtype EP4) (PTGER4) interaction partners

1. Data suggest that lysophosphatidic acid (LPA) up-regulates expression of SLCO2A1 (prostaglandin [PG] transporter), PTGER2/PTGER4 (PG receptors EP2/EP4), and mPGES1/cPGES (microsomal/cytosolic PG E synthases) in luteal cells.

2. Data suggest that estradiol up-regulates mRNA and protein expression of 3 prostanoid receptors in oviduct smooth muscle: EP2/PTGER2 (prostaglandin E receptor 2); EP4/PTGER4 (prostaglandin E receptor 4); and FP/PTGFR (prostaglandin F2alpha receptor).

3. The PGE2-mediated down-regulation of CD25 expression on T cells is mediated via the EP4 receptor, although selective activation of the EP2 receptor up-regulates the CD25 expression on these cells.

4. EP4 is undetectable in endometrium and myometrium during the estrous cycle

5. Quantitative RT-PCR revealed significant higher expression of EP2 and EP4 in the pre-ovulatory phase compared with the luteal phase in the bovine oviduct