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EP2 Subtype Prostaglandin E Receptors

A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES.
Also Known As:
Receptors, Prostaglandin E, EP2 Subtype; PGE Receptor, EP2 Subtype; Prostaglandin E Receptor 2; Prostanoid Receptor EP2; EP2, Prostanoid Receptor; Receptor EP2, Prostanoid
Networked: 27 relevant articles (0 outcomes, 4 trials/studies)

Bio-Agent Context: Research Results

Experts

1. Che, Lihe: 1 article (12/2021)
2. Dong, Dan: 1 article (12/2021)
3. Du, Na: 1 article (12/2021)
4. Li, Xiaohua: 1 article (12/2021)
5. Liu, Yong: 1 article (12/2021)
6. Sun, Luyao: 1 article (12/2021)
7. Wang, Bin: 1 article (12/2021)
8. Chen, Ting-Ting: 1 article (01/2020)
9. Du, Jia-Jia: 1 article (01/2020)
10. Li, Nan: 1 article (01/2020)

Related Diseases

1. Prostatic Neoplasms (Prostate Cancer)
2. Ovarian Neoplasms (Ovarian Cancer)
3. Carcinoma (Carcinomatosis)
4. Breast Neoplasms (Breast Cancer)
5. Inflammation (Inflammations)
01/01/2017 - "Among each PG receptor subtype examined, prostaglandin E receptor 2 (EP2) signaling specifically contributes to colorectal cancer formation and inflammation in lesions of AOM-DSS model. "
09/01/2019 - "2ccPA treatment also decreased the amount of prostaglandin E2 (PGE2) produced by LPS-stimulated THP-1 cells and decreased expression of the mRNA of prostaglandin E receptor 2 (EP2, PTGER2), a PGE2 receptor that mediates inflammation. "
11/01/2012 - "We previously reported that prostaglandin (PG) E2 acts as a ligand for prostaglandin E receptor 3 (EP3) in conjunctival epithelial cells, that it downregulates the progression of experimental murine allergic conjunctivitis, and that in human conjunctival epithelial cells it modulates the expression of polyI:C-induced proinflammatory genes via prostaglandin E receptor 2 (EP2) and EP3, suggesting that PGE2 might have important roles in ocular surface inflammation such as allergic conjunctivitis. "
01/01/2019 - "Measurements and Main Results: Group-level analyses demonstrated that infant peripheral blood mononuclear cell responses were dominated by monocyte-associated hyperupregulated type 1 IFN signaling/proinflammatory pathways (drivers: TNF [tumor necrosis factor], IL-6, TREM1 [triggering receptor expressed on myeloid cells 1], and IL-1B), versus a combination of inflammation (PTGER2 [prostaglandin E receptor 2] and IL-6) plus growth/repair/remodeling pathways (ERBB2 [erbb-b2 receptor tyrosine kinase 2], TGFB1 [transforming growth factor-β1], AREG [amphiregulin], and HGF [hepatocyte growth factor]) coupled with T-helper cell type 2 and natural killer cell signaling in children. "

Related Drugs and Biologics

1. Dinoprostone (PGE2)
2. Interleukin-6 (Interleukin 6)
3. ErbB Receptors (EGF Receptor)
4. Cyclooxygenase 2 (Cyclooxygenase-2)
5. Messenger RNA (mRNA)
6. Prostaglandins
7. Prostaglandin-Endoperoxide Synthases (Cyclooxygenase)
8. Amphiregulin
9. EP3 Subtype Prostaglandin E Receptors
10. Receptor Protein-Tyrosine Kinases (Tyrosine Kinase Receptors)