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This study showed that COX-1 (show PTGS1 Proteins) and COX-2 in genital carcinomas in the horse is poor; microsomal PGES (show PTGES Proteins)-1 is more prominently expressed.
Progestin treatment does not affect expression of cytokines, steroid receptors, oxytocin receptor (show OXTR Proteins), and cyclooxygenase 2 in fetal membranes and endometrium.
COX-1 (show PTGS1 Proteins) and COX-2 genes were constitutively expressed in baseline samples. Low-flow ischemia resulted in significant upregulation of COX-2 gene expression at each subsequent time point, compared with baseline values.
The role for p38 (show MAPK14 Proteins) mitogen-activated kinase (MAPK (show MAPK1 Proteins)) in the signaling mechanism regulating pro-inflammatory cyclooxygenase (COX (show CPOX Proteins)) gene expression in lipopolysaccharide (LPS (show IRF6 Proteins))-activated equine leukocytes in horses is reported.
In this study, both COX-1 (show PTGS1 Proteins) and COX-2 were expressed in the colon before induced ischemia; ischemic injury increased expression of COX-2.
Immunoreactivity for COX-1 (show PTGS1 Proteins) and COX-2 is high in equine corneal SCC (show CYP11A1 Proteins), possibly indicating that COX (show CPOX Proteins) plays a role in oncogenesis or progression of this tumor type at this site.
It was found that most equine squamous-cell carcinomas and many melanomas appear to express COX-2 and thus could respond to COX-2 inhibitor therapy.
data support the hypothesis that prostaglandin G/H synthase 2(PGHS2)is a target for the antiluteolytic signal produced by equine conceptuses during early pregnancy
The objective of this study was to evaluate the mRNA expression of prostaglandin-endoperoxide synthase 2 (PTGS 2), prostaglandin F2alpha synthase (PTGFS) and prostaglandin E2 microsomal synthase 1 (mPTGES 1) in the endometrium of repeat-breeding cows with and without subclinical endometritis.
results indicate that nuclear receptor subfamily 1 group D member 1(REV-ERBalpha (show NR1D1 Proteins)) plays an inhibitory role in the expression of prostaglandin-endoperoxide synthase 2(PTGS2) in both bovine USCs and UECs treated with ovarian steroids
This study showed that neutrophils from periparturient heifers show impairment of COX-2 mRNA expression and lactoferrin (show LTF Proteins), suggesting that these mechanisms may contribute to immunosuppression in cows around calving.
Exposure to follicular fluid transiently increased the transcript levels of IL8 (show IL8 Proteins) and PTGS2, and decreased the expression of SOD2 (show SOD2 Proteins), GPX3 (show GPX3 Proteins), DAB2 (show DAB2 Proteins), and NR3C1 (show NR3C1 Proteins). TNF (show TNF Proteins) and IL6 (show IL6 Proteins) levels were also decreased while those of NAMPT (show NAMPT Proteins) were unaffected.
Purinergic P2Y1 receptor (show P2RY1 Proteins) signaling mediates wound stimuli-induced cyclooxygenase-2 expression in intestinal subepithelial myofibroblasts
Data suggest that Escherichia coli infections (here, administration of LPS (show IRF6 Proteins)) provokes luteolysis in diestrus, non-lactating cows but no change in expression of PTGS2 in corpus luteum and has no effect on luteinization in the following cycle.
This study is the first to report the involvement of PGE2 in oocyte MAPK (show MAPK1 Proteins) activation during the maturation process.
Inhibitors of c-Src (show SRC Proteins) (PP2, 10 microm) and PI3K (LY294002, 25 microm) produced a significant decrease in oxytocin-induced PGF (show PGF Proteins)(2 alpha) production and reduced COX2 expression by endometrial epithelial cells.
COX-2 pathway is responsible for the endometrial production of PGE (show LIPF Proteins)(2) in the bovine endometrium during the estrous cycle
the conceptus, through its secretion of IFN-tau, stimulates maternal epithelial expression of COX-2 and GM-CSF (show CSF2 Proteins) during the peri (show PLIN1 Proteins)-attachment period in the cow.
Angiotensin II-AT1-receptor (show AGTRAP Proteins) signaling is necessary for COX-2-dependent normal postnatal nephrogenesis and maturation.
AhR (show AHR Proteins) controls COX-2 protein via mRNA stability.
Podocyte-specific knockout of COX2 enhanced albuminuria and did not attenuate the histologic features of diabetic kidney disease.
Salt supplementation during the COX-2-dependent time frame of nephrogenesis partly reverses renal morphological defects in COX-2(-/-) mice and improves kidney function.
Data suggest that induction of Ptgs2 expression in preimplantation uterus may be earliest positive embryo/blastocyst signal for implantation and pregnancy recognition in mice.
the bone regeneration capacity of Cox (show CPOX Proteins)-2KO MDSCs was impaired because of a reduction in cell proliferation and survival capacities, reduction in osteogenic differentiation and a decrease in the ability of the cells to recruit host cells to the injury site.
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.
Data (including data from studies using knockout/mutant mice) suggest that Mir200c (microRNA 200c) is involved in endothelial function/dysfunction via regulation of Cox2 (cyclooxygenase-2) expression; overexpression of Mir200c impairs endothelium-dependent vascular relaxation (EDVR) in non-diabetic mouse aorta, whereas suppression of Mir200c by anti-Mir200c enhances EDVR in diabetic mouse aorta.
data indicate that excessive adipocyte lipolysis activates the JNK (show MAPK8 Proteins)/NFkappaB pathway leading to the up-regulation of COX-2 expression and recruitment of inflammatory macrophages.
this study shows that c-Jun (show JUN Proteins) regulates the activation state of macrophages and promotes arthritis via differentially regulating cyclooxygenase-2 and arginase-1 (show ARG1 Proteins) levels
that a genetically modulated balancing of signaling within the CB1 (show CNR1 Proteins)-COX-2 pathway may reflect on more or less efficient patterns of prefrontal activity during working memory
Diabetes and cardiopulmonary bypass are associated with upregulation in COX-2 expression/activation in peripheral microvasculature.
COX-2 directly oxidizes 2-arachidonoyl-lysophospholipids to eicosanoid-lysolipids.
COX-2 is a potential marker for identifying high-risk sebaceous gland carcinoma (SGC (show SGCB Proteins)) patients. Expression of PPAR-gamma (show PPARG Proteins) in eyelid SGC (show SGCB Proteins) cases reflects terminal sebaceous differentiation.
COX-2 expression correlates with and modulates PD-L1 (show CD274 Proteins) expression in melanoma cells.
PTGS2 rs20417CC genotype is associated with carotid plaque vulnerability, platelet activation and TXA2 (show TBXA2R Proteins) levels in ischemic stroke patients.
Current results suggest that COX-2 rs689466, rs5275, and rs20417 polymorphisms are not associated with head and neck squamous cell carcinoma.[meta-analysis]
Specific inhibitors of COX-2 and 5-LOX (show ALOX5 Proteins) decreased formation of HKD2 and HKE2 (show PFDN6 Proteins) Platelets did not form HKs from exogenous 5S-hydroxyeicosatetraenoic acid, implying that COX-1 is not involved
Leptin (show LEP Proteins) induced COX-2 expression, promoter activity, and increased the production of prostaglandin E2.
These findings suggest that nuclear factor kappa B(NF-kappaB (show NFKB1 Proteins)) and cyclooxygenase-2 play roles in epidermal cell regeneration following beta-irradiation of mini-pig skin.
COX2 expression is upregulated in CAVD, and its activity contributes to osteogenic gene induction and valve calcification in vitro and in vivo.
These results suggest that COX-2 plays a role in the pathogenesis of Mycoplasma hyopneumoniae -infection.
Brain death increases the expression of COX-1 and COX-2 mRNA in the renal medulla
COX-2 is differentially expressed in normal versus lungworm-infected lungs of pigs and is likely to be involved in the pathogenesis of porcine parasitic bronchopneumonia.
In porcine vas (show AVP Proteins) deferens epithelial cell monolayers, increases in anion secretion were associated with preferential upregulation of PTGS2 at the mRNA and protein levels.
expression appears to be positively and negatively regulated by p38 MAPK (show MAPK14 Proteins) and JNK (show MAPK8 Proteins) pathways; alternatively, ERK1/2 appear to be involved in COX-2-independent reparative events that remain to be defined
Neutrophils augment recovery of transepithelial electrical resistance in ischemia-injured ileal mucosa via IL-1beta (show IL1B Proteins)-dependent upregulation of COX-2. (Cyclooxygenase 2)
Administration of estrogen early in pregnancy alters endometrial prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA and protein expression, which may disrupt pregnancy causing total embryonic loss during implantation in the pig.
The effect of EGF (show EGF Proteins) on pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha (show TNF Proteins)) and cyclooxygenase-2 (COX-2), levels during wound healing in swine is reported.
results revealed that a transient episode of raised-intensity phonation causes a significant increase in vocal fold inflammatory mRNA expression - IL-1beta (show IL1B Proteins),COX-2, and TGFbeta1 (show TGFB1 Proteins)
The result demonstrate that mechanical stress on synovial cells induces gene expressions of COX-2.
Diabetes enhances the vasodilator response of the rabbit carotid artery to testosterone by a mechanism that includes an increased modulatory activity of the endothelial nitric oxide and an augmented release of COX-2 vasodilator, prostacyclin.
Local induction of COX-2 during atherosclerosis decreased the sensitivity to norepinephrine and that COX-2 inhibitors may increase vascular reactivity at sites of atherosclerotic lesions.
The vesicular gland of castrated goats showed significantly lower AR and COX-2 immuno-expression than intact goats indicating that both AR and COX-2 are androgen dependent.
Prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase, is the key enzyme in prostaglandin biosynthesis, and acts both as a dioxygenase and as a peroxidase. There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2, which differ in their regulation of expression and tissue distribution. This gene encodes the inducible isozyme. It is regulated by specific stimulatory events, suggesting that it is responsible for the prostanoid biosynthesis involved in inflammation and mitogenesis.
PGH synthase 2
, PHS II
, cyclooxygenase 2b
, prostaglandin G/H synthase 2
, prostaglandin H2 synthase 2
, cyclooxygenase 2
, glucocorticoid-regulated inflammatory cyclooxygenase
, macrophage activation-associated marker protein P71/73
, prostaglandin G/H synthase and cyclooxygenase
, mitogen-inducible PGHS
, cyclooxygenase type 2
, prostaglandin G/H synthase-2
, cyclooxygenase, prostaglandin endoperoxide H synthase-2
, prostaglandin H synthase-2
, prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)
, prostaglandin G/H synthase 2-like