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The protein encoded by PTGES is a glutathione-dependent prostaglandin E synthase. Additionally we are shipping Prostaglandin E Synthase Antibodies (58) and Prostaglandin E Synthase Kits (22) and many more products for this protein.
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COX-2 and mPGES-1-dependent synthesis of PGE2 contributes to a dedifferentiated aortic smooth muscle cell phenotype.
Several studies provide evidence that the expression of mPGES1 is regulated by a number of transcriptional factors and inducible in conditions of inflammation and hypoxia.[review]
The Genome Wide Area Study, using a phenotyping algorithm for asthma for data mining electronic medical records, identified four asthma susceptibility loci: 6p21.31, 9p21.2, and 10q21.3 in the European American population; and the prostaglandin synthase E gene (PTGES) at 9q34.11 in African Americans. Biologic support exists for genes at the 9p21.2 and 9q34.11 loci TEK (show TEK Proteins), encoding the endothelial tyrosine in animal studies.
C-myc (show MYC Proteins) regulates mPGES1 expression by binding to the proximal promoter. C-myc (show MYC Proteins) transfection in HeLa cells up-regulates mPGES1 mRNA and protein expression.
COX-2 and mPGES-1 have roles in arachidonic acid regulation of inflammatory prostaglandin E2 biosynthesis
The identified amino acid residues can act as target sites for the design and development of drug candidates against mPGES-1
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) and microsomal PGE (show LIPF Proteins) synthase-1 (mPGES-1) dependent pathway.
Data show that cyclooxygenase2 (COX2)overexpression induces prostaglandin E synthase (PTGES) through early growth response 1 (EGR1 (show EGR1 Proteins)) in colorectal cancer cell lines.
mPGES-1 is downregulated via EGR1 (show EGR1 Proteins) and has a role in caffeine inhibition on PGE2 synthesis of HBx hepatocytes
that mPGES-1 exerts a potentially protective effect against renal fibrosis and inflammation induced by unilateral ureteral obstruction in mice
In line with the acetyltransferase activity of p300 (show NOTCH1 Proteins), H3K27 acetylation was reduced after HDACi and resulted in the formation of heterochromatin in the PTGES1 gene. In conclusion, HDAC (show HDAC3 Proteins) activity maintains PTGES1 expression by recruiting p300 (show NOTCH1 Proteins) to its gene
The findings suggest that COX-2/mPGES-1/PGE2 axis could be activated by albumin (show ALB Proteins) in the proximal tubular cells via a NLRP3 (show NLRP3 Proteins) inflammasome-mediated mechanism and could thus contribute to proteinuria-related renal tubular cell injury.
mPGES-1 overexpression prevents Fas (show FAS Proteins)-induced hepatocyte apoptosis and liver injury through activation of Akt (show AKT1 Proteins) .
The expression of Lcn2 (show LCN2 Proteins) and mPGES-1 is strongly stimulated by lipopolysaccharide (LPS (show TLR4 Proteins)), indicating that Lcn2 (show LCN2 Proteins) mediates LPS (show TLR4 Proteins)-induced inflammation. These findings shed light on the role of Lcn2 (show LCN2 Proteins) during decidualization.
The results show that mPges-1 may be a direct downstream target gene of the P4 receptor (show PGR Proteins).
mPges-1 depletion modestly increased thrombogenesis in LDL-receptor (show LDLR Proteins) 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 Proteins) and prostaglandin E synthase-1 cooperatively exacerbate inflammatory reactions but have opposing effects on carcinogenesis.
Gas6 (show GAS6 Proteins), through upregulation of Ptges/PGE2, contributes to cancer-induced venous thrombosis.
The objective of this study was to evaluate the mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS 2 (show PTGS2 Proteins)), prostaglandin F2alpha synthase (PTGFS) and prostaglandin E2 microsomal synthase 1 (mPTGES 1) in the endometrium of repeat-breeding cows with and without subclinical endometritis.
Prostaglandin E synthase interacts with inducible heat shock protein 70 (show HSPA1A Proteins) 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 Proteins)) and Fas (show FAS Proteins) 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 Proteins) (heat shock 90 kD protein 1 alpha).
PGES pathway is responsible for the endometrial production of PGE (show LIPF Proteins)(2) in the bovine endometrium during the estrous cycle
This study showed that COX-1 (show PTGS1 Proteins) and COX-2 (show PTGS2 Proteins) 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