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The protein encoded by PTGES is a glutathione-dependent prostaglandin E synthase. Additionally we are shipping Prostaglandin E Synthase Kits (19) and Prostaglandin E Synthase Proteins (6) and many more products for this protein.
Showing 10 out of 56 products:
Human Polyclonal Prostaglandin E Synthase Primary Antibody for IHC, IHC (p) - ABIN4347784
Camacho, Dilmé, Solà-Villà, Rodríguez, Bellmunt, Siguero, Alcolea, Romero, Escudero, Martínez-González, Vila: Microvascular COX-2/mPGES-1/EP-4 axis in human abdominal aortic aneurysm. in Journal of lipid research 2013
Show all 4 references for ABIN4347784
These findings support the value of a prognostic and predictive role for mPGES1.
Data show that statins limit hepatic myofibroblasts proliferation via a cyclooxyegnase-2 (COX-2 (show COX2 Antibodies)) and microsomal PGE (show LIPF Antibodies) synthase-1 (mPGES-1) dependent pathway.
Data show that cyclooxygenase2 (COX2 (show COX2 Antibodies))overexpression induces prostaglandin E synthase (PTGES) through early growth response 1 (EGR1 (show EGR1 Antibodies)) in colorectal cancer cell lines.
mPGES-1 is downregulated via EGR1 (show EGR1 Antibodies) and has a role in caffeine inhibition on PGE2 synthesis of HBx hepatocytes
results demonstrate that mPGES-1 is a target gene of defective mismatch repair in human colorectal cancer, with functional consequence
Altered expression of EP2 (show SPAG11B Antibodies) in patients with aspirin-exacerbated respiratory disease contributes to deficient induction of IL-1RI, reducing the capacity of IL-1beta (show IL1B Antibodies) to increase COX-2 (show COX2 Antibodies) and mPGES-1 expression, which results in low PGE2 production
High levels of intra tumoral mPGES-1 is associated with poor prognosis. mPGES-1 after chemotherapy is associated with improved outcomes.
mPGES-1 in prostate cancer controls stemness and amplifies epidermal growth factor receptor (show EGFR Antibodies)-driven oncogenicity
we investigated the changes in promoter methylation patterns using methylation arrays and observed that the promoters of immunomodulatory factors, COX2 (show COX2 Antibodies) and PTGES, and migration-related factors, CXCR2 (show CXCR2 Antibodies) and CXCR4 (show CXCR4 Antibodies), were hypomethylated after 5-aza treatment
Data suggest that, in organization of enzymes in post-translational endoplasmic reticulum, mPGES1 is likely co-localized with COX2 (cyclooxygenase-2 (show PTGS2 Antibodies)) within a distance of 14.4 A; mPGES-1 is localized much farther from COX1 (cyclooxygenase-1 (show PTGS1 Antibodies)).
mPges-1 depletion modestly increased thrombogenesis in LDL-receptor (show LDLR Antibodies) knockout mice. This response was markedly further augmented by coincident deletion of the I prostanoid receptor.
Data (including data from studies in knockout mice) suggest interactions of cholinergic/prostaglandin systems participate in neuroimmunomodulation; microsomal Ptges-1 is part of cholinergic anti-inflammatory response in chronic inflammatory diseases.
Prostacyclin synthase (show PTGIS Antibodies) and prostaglandin E synthase-1 cooperatively exacerbate inflammatory reactions but have opposing effects on carcinogenesis.
Gas6 (show GAS6 Antibodies), through upregulation of Ptges/PGE2, contributes to cancer-induced venous thrombosis.
Vascular mPGES-1 plays a protective role in blood vessels and attenuates rupture of cerebral aneurysms.
Suggest pivotal role of COX-2 (show COX2 Antibodies)-mPGES-1-PGE2 axis in vascular calcification. Inhibition of COX-2 (show COX2 Antibodies) or mPGES-1 may increase the risk of calcification and subsequent adverse cardiovascular events during chronic renal failure.
The present results suggest that mPGES-1 plays a significant role in lymphangiogenesis during inflammation, and represents a novel target for controlling IL.
data suggests that an as yet unidentified prostaglanind E synthase but not mPGES-1 may couple with COX-2 (show COX2 Antibodies) to mediate increased renal PGE2 sythsesis in DN.
This study shown that mPGES-1 is expressed in the mouse brain, both in vascular endothelial cells, in several other cellular of capillary associated pericytes, astrocytes, and cells in circumventricular organs, choroid plexus, and leptomeninges.
mPGES-1 deficiency exacerbates bleomycin-induced pulmonary fibrosis.
Prostaglandin E synthase interacts with inducible heat shock protein 70 (show HSPA1A Antibodies) after heat stress in bovine primary dermal fibroblast cells.
Messenger RNA and protein levels of prostaglandin (PG) E synthase (PGES), PGF2alpha receptor (PGFR), tumor necrosis factor-alpha (TNF (show TNF Antibodies)) and Fas (show FAS Antibodies) were found to be higher in the corpus luteum of pregnancy than in corpus luteum of the cycle.
Data suggest that elevated temperatures stimulate PGE2 production in ampullary oviduct by increasing expression of PGES and HSP90AA1 (show HSP90AA1 Antibodies) (heat shock 90 kD protein 1 alpha).
PGES pathway is responsible for the endometrial production of PGE (show LIPF Antibodies)(2) in the bovine endometrium during the estrous cycle
This study showed that COX-1 (show PTGS1 Antibodies) and COX-2 (show PTGS2 Antibodies) in genital carcinomas in the horse is poor; microsomal PGES-1 is more prominently expressed.
The protein encoded by this gene is a glutathione-dependent prostaglandin E synthase. The expression of this gene has been shown to be induced by proinflammatory cytokine interleukin 1 beta (IL1B). Its expression can also be induced by tumor suppressor protein TP53, and may be involved in TP53 induced apoptosis. Knockout studies in mice suggest that this gene may contribute to the pathogenesis of collagen-induced arthritis and mediate acute pain during inflammatory responses.
microsomal prostaglandin E synthase-1
, prostaglandin E synthase
, MGST1-like 1
, glutathione S-transferase 1-like 1
, microsomal glutathione S-transferase 1-like 1
, microsomal prostaglandin E synthase 1
, p53-induced apoptosis protein 12
, p53-induced gene 12 protein
, tumor protein p53 inducible protein 12