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Human Prostaglandin E Synthase 2 (PTGES2) interaction partners

1. Four single nucleotide polymorphisms in two genes in the PGE2 family, PTGES2 and PTGER4, were significantly associated with primary graft dysfunction after lung transplantation.

2. high immunoreactivity of mPGES-2 in pyramidal neurons of AD brains indicates that it might have a potential role in the functional replacement of cytosolic PGES or inactive mPGES-1 in later stages of Alzheimer disease

3. Up-regulation of prostaglandin E2 synthesis by interleukin-1beta in human orbital fibroblasts involves coordinate induction of prostaglandin-endoperoxide H synthase-2 and glutathione-dependent prostaglandin E2 synthase expression

4. role in regulating interferon-gamma-dependent gene expression

5. 110Cys is essential in the active site of membrane-associated prostaglandin E synthase-2

6. Transactivators GBF1 and CCAAT/enhancer-binding protein-beta physically interact to induce interferon-gamma-regulated transcription; a 37-aa long peptide derived from the GBF1 protein can associate with C/EBP-beta in an IFN-inducible manner.

7. alphaTOS inhibits COX activity, thereby inhibiting PGE2 production in human lung epithelial cells

8. study obtained evidence from two Caucasian study populations that the His298-allele of PTGES2 Arg298His confers to reduced risk of type 2 diabetes

9. Carbonyl reductase-1 (CBR1), microsomal prostaglandin E synthase-1 and 2 (mPGES-1, mPGES-2), cytosolic prostaglandin E synthase (cPGES), aldoketoreductase (AKR1C1) and prostaglandin F synthase (AKR1C3) were all expressed in hair follicles.

10. risk-reducing effects of the minor His allele of the prostaglandin E synthase 2 (PTGES2) Arg298His polymorphism could be mediated partly by lowered body mass index (BMI)

11. all three terminal prostaglandin synthases, mPGES-1, mPGES-2, and cPGES, are over-expressed in human gliomas

12. A marginal but significant influence of the PTGES2 298H single nucleotide polymorphism on BMI was found in a large population-based study.

13. These results indicate that mPGES-1 and mPGES-2 may each play a role in colorectal cancer progression.

Mouse (Murine) Prostaglandin E Synthase 2 (PTGES2) interaction partners

1. mPGES-2 deletion enhanced streptozotocin (STZ)-induced liver toxicity possibly via GLUT2-mediated STZ uptake, independently of diabetes mellitus in mice.

2. increased expression of miR-146a in bone marrow-derived mesenchymal stem cells correlated with inhibition of prostaglandin E2 synthase-2 and inhibition of prostaglandin E2 release.

3. Transactivators GBF1 and CCAAT/enhancer-binding protein-beta physically interact to induce interferon-gamma-regulated transcription; a 37-aa long peptide derived from the GBF1 protein can associate with C/EBP-beta in an IFN-inducible manner.

4. In the urogenital system, membrane-associated PGES-2 was highly expressed in the renal cortex, followed by the renal medulla and ovary, with lower levels in the ureter, bladder and uterus.

5. Study suggests that in hypertensive mice, there are (a) significant microanatomic variations in the pulmonary, renal, and cardiac distribution and cellular localization of mPGES-2 and no differences in expression between genders.

6. Analysis of the mPGES-2 deficient mouse lines does not substantiate the contention that mPGES-2 is a PGE(2) synthase.

7. This article reviews the involvement of the PGE(2), Wnt, and BMP pathways in the development of gastric cancer.

8. PGE(2) protects the pulmonary vasculature from remodeling during allergen-induced pulmonary inflammation