Use your antibodies-online credentials, if available.
抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
Human Polyclonal PTGS2 Primary Antibody for IHC (p), WB - ABIN3044295
Guo, Li, Wu, Gong, Lu, Shi: Protective effects of icariin on brain dysfunction induced by lipopolysaccharide in rats. in Phytomedicine : international journal of phytotherapy and phytopharmacology 2010
Show all 32 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for IHC (fro), IHC (p) - ABIN3044296
Liu, Yan, Li, Yin, Sun, Kou, Ye, Ferns, Liu, Liu: Reduced expression of SOX7 in ovarian cancer: a novel tumor suppressor through the Wnt/?-catenin signaling pathway. in Journal of ovarian research 2014
Show all 31 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for WB - ABIN5518867
Wang, Du, Wang, Kuang, Wang: Z-ligustilide attenuates lipopolysaccharide-induced proinflammatory response via inhibiting NF-kappaB pathway in primary rat microglia. in Acta pharmacologica Sinica 2010
Show all 19 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for IHC, IHC (p) - ABIN152112
Chu, Yeh, Lin, Jung, Ma, Wang, Wu, Shiu, Chen: Deletion of the FHL2 gene attenuating neovascularization after corneal injury. in Investigative ophthalmology & visual science 2008
Show all 16 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for IF (p), IHC (p) - ABIN672471
Gao, Wen, Yang, Lu, Tong, Huang, Liu, Tang: Celecoxib ameliorates portal hypertension of the cirrhotic rats through the dual inhibitory effects on the intrahepatic fibrosis and angiogenesis. in PLoS ONE 2013
Show all 10 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for ELISA, WB - ABIN257712
George, Morrow, Xu, Yi, Holmes, Wu, Li, Protter, Oz, Wang: Prolonged effects of B-type natriuretic peptide infusion on cardiac remodeling after sustained myocardial injury. in American journal of physiology. Heart and circulatory physiology 2009
Show all 4 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for IHC (p), WB - ABIN965923
Salmenkivi, Haglund, Ristimäki, Arola, Heikkilä: Increased expression of cyclooxygenase-2 in malignant pheochromocytomas. in The Journal of clinical endocrinology and metabolism 2001
Show all 4 Pubmed References
Polyclonal PTGS2 Primary Antibody for IHC (p), WB - ABIN540585
Liu, Chang, Narko, Trifan, Wu, Smith, Haudenschild, Lane, Hla: Overexpression of cyclooxygenase-2 is sufficient to induce tumorigenesis in transgenic mice. in The Journal of biological chemistry 2001
Show all 3 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for WB - ABIN6146415
Dai, Ciccotosto, Cappai, Tang, Li, Xie, Xiao, Velkov: Curcumin Attenuates Colistin-Induced Neurotoxicity in N2a Cells via Anti-inflammatory Activity, Suppression of Oxidative Stress, and Apoptosis. in Molecular neurobiology 2018
Show all 3 Pubmed References
Human Polyclonal PTGS2 Primary Antibody for WB - ABIN6685998
Zhang, Li, Li, Liu, Wei, Qian: Ceramide enhances COX-2 expression and VSMC contractile hyperreactivity via ER stress signal activation. in Vascular pharmacology 2017
Show all 3 Pubmed References
The expression of COX-2 increase with stage of the endometrial tumor and with the expression of p53 and VEGF in the endometrial carcinomas.
COX2-765 GG genotype is associated with vitiligo, especially of the generalized type. COX2-1195A/G gene polymorphism is not associated with the risk of developing vitiligo or with vitiligo subtypes.
dysregulation of PAX5/PTGS2 cascade plays a causal role in the induction of Cisplatin resistance
The majority of GEP-NETs over express cox-2 gene.
COX2, -765, -1195 polymorphisms appear to be an important predictive factor and may be a prognostic biomarker for risk of Oral squamous cell carcinoma.
VEGF, COX-2, and p27 may be important biological markers that determine the angiogenic and lymphangiogenic potentials of papillary thyroid carcinoma, particularly between the follicular and classic variants.
SND1 may act as a potential biomarker of the therapeutic strategies utilizing COX2 inhibitors.
Authors showed that mRNA and protein levels of COX2 and HER2 were upregulated in CRC compared with the adjacent tissues. COX2 protein levels and nuclear COX2 expression were correlated with a poor prognosis of CRC patients. COX2 expression was positively associated with HER2 expression.
PTGS2 polymorphisms were associated with advanced liver fibrosis in patients with HCV mono-Infection and HCV/HIV Co-Infection.
An unrecognized cellular interaction between follicular dendritic cells and B cells leading to COX-2 expression during immune inflammatory responses.
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in Alzheimer's disease patients and in a transgenic mouse model.
miR-137 suppresses the proliferation and invasion of retinoblastoma cells by targeting COX-2/PGE2 signaling pathway.
Dual governing of YAP and COX-2 may lead to the discovery of promising therapeutic strategies for HCC patients.
COX-2 expression was positively associated with the recurrence and a poor prognosis of patients with nasopharyngeal carcinoma.
COX-2 is an important factor for Dengue virus replication.
Lysophosphatidylcholine induces COX-2-mediated IL-6 expression. NADPH oxidase/Reactive Oxygen Species is involved in Lysophosphatidylcholine-induced COX-2 expression.
results support a critical role of ATF6alpha in the establishment and maintenance of cellular senescence in normal human fibroblasts via the up-regulation of a COX2/PGE2 intracrine pathway.
High PTGS2 expression is associated with Breast Carcinoma.
concluded that COX-2 gene rs5275 variant contributes to Nasopharyngeal carcinoma risk in a Chinese population
COX2 and YAP1 signaling pathways are connected with each other to induce SOX2 expression, cancer stem cell enrichment, and acquired resistance to chemotherapy in urothelial carcinoma of the bladder.
Protein phosphorylation of tyrosine residues plays an important role in the regulation of expression and glycosylation during 2DG-induced ER stress in rabbit articular chondrocytes.
results revealed that a transient episode of raised-intensity phonation causes a significant increase in vocal fold inflammatory mRNA expression - IL-1beta,COX-2, and TGFbeta1
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.
These findings suggest that nuclear factor kappa B(NF-kappaB) 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
COC-2 inhibitors did not decrease collateral-dependent blood flow to the myocardium in a model of chronic myocardial ischemia.
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 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 and JNK 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-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 on pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase-2 (COX-2), levels during wound healing in swine is reported.
myocardial infarction induced proinflammatory gene and protein expression in peripheral blood mononuclear cells of tissue factor cyclo-oxygenase-2, monocyte chemoattractant protein-1 and CRP
constitutive hepatocyte COX-2 expression ameliorates NASH and liver fibrosis development by reducing inflammation, oxidative stress and apoptosis and by modulating activation of hepatic stellate cells
These data indicate that the COX-2/PGE2 signaling pathway has proviral effects for the replication of FCV and MNV, and pharmacological inhibitors against these enzymes serve as potential therapeutic candidates for treating FCV and MNV infections.
These results suggest a crucial role for the COX-2 signaling pathway in the intermittent hypoxia-exacerbated malignant processes, and designate macrophages and lung adenocarcinoma cells, as potential sources of prostaglandin E2.
Results demonstrate that neither the basal nor seizure-induced expression profiles of COX-2 were altered in mice lacking a functional TIA-1 gene suggesting that TIA-1 does not contribute to regulation of COX-2 protein expression in neurons. Induced seizure threshold was also unchanged in mice lacking TIA-1 protein, indicating that this RNA binding protein does not influence the innate seizure threshold.
The kidney is the principle site in the body where local COX-2 controls blood flow via PPARbeta/delta-mediated renal vasodilator pathway.
Mitochondrial catalase induces neoplastic cell transformation through nucleolin-dependent Cox-2 mRNA stabilization.
The COX2-dependent lipid inflammatory pathway is responsible for lethality in F. novicida infection due to overproduction of proinflammatory effectors including prostaglandin E2.
These data indicate the functional role of the MIF-COX-p53 axis in inflammation and cancer at the genomic and proteomic levels in COX-2-ablated cells.
PTGS2 deletion changes the natural distribution of ANXA2 in monocytes/macrophages, increasing TF expression and activity predisposing to venous thrombosis.
Study suggest that amyloid beta-protein increase the expression of TRPC6 via NF-kappaB in BV-2 microglia and promotes the production of COX-2, which induces hippocampus neuron damage.
Data show that patients with high cyclooxygenase-2 (COX2) gene expression who received celecoxib had a significantly higherpathological complete response (pCR) rate compared with patients with low COX2 gene expression.
Topical application of glycolic acid suppresses the UVB induced IL-6, IL-8, MCP-1 and COX-2 inflammation by modulating NF-kappaB signaling pathway in mouse skin.
COX-2/mPGES-1/PGE2 cascade activation mediates uric acid-induced glomerular mesangial cell proliferation.
Cobalt protoporphyrin induces COX-2 expression through activating P2X7 receptors and ASK1/MAP kinases as well as PIAS1 degradation signaling pathways.
sUV activated the transcription factors nuclear factor-kappaB and activator protein-1 which, in turn, induces COX-2 expression.
Results indicate that Cox-2 promotes Col10a1 expression and chondrocyte hypertrophy in vitro.
These data reveal important structure-function and signaling differences between the two FFA4 isoforms, and for the first time link FFA4 to modulation of ROS in macrophages.
Our data suggest that there are physiologically important gender differences in hypoxic acclimatization in COX-2-deficient mice. The COX-2 signaling pathway appears to be required for acclimatization in oxygen-limiting environments only in males, whereas female COX-2-deficient mice may be able to access COX-2-independent mechanisms to achieve hypoxic acclimatization.
Data suggested that PTGS-2 gene expression was induced by PTGER2 activation through the PKA and ERK pathways.
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) 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, suggesting that these mechanisms may contribute to immunosuppression in cows around calving.
Exposure to follicular fluid transiently increased the transcript levels of IL8 and PTGS2, and decreased the expression of SOD2, GPX3, DAB2, and NR3C1. TNF and IL6 levels were also decreased while those of NAMPT were unaffected.
Purinergic P2Y1 receptor signaling mediates wound stimuli-induced cyclooxygenase-2 expression in intestinal subepithelial myofibroblasts
Data suggest that Escherichia coli infections (here, administration of LPS) 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 shows that 9-cis retinoic acid can exert its beneficial effect on parthenogenetic embryo production in pigs by multidimensional pathways affecting oocyte maturation.
This study is the first to report the involvement of PGE2 in oocyte MAPK activation during the maturation process.
Inhibitors of c-Src (PP2, 10 microm) and PI3K (LY294002, 25 microm) produced a significant decrease in oxytocin-induced PGF(2 alpha) production and reduced COX2 expression by endometrial epithelial cells.
COX-2 pathway is responsible for the endometrial production of PGE(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 during the peri-attachment period in the cow.
the PGHS-2 promoter is regulated by bovine upstream stimulatory factor 1 and 2 in preovulatory granulosa cells
Activation of p38 MAPK by PdBu is required for continued presence of PGHS-2 mRNA and secretion of prostaglandin F(2alpha) in BEND cells. Interferon-tau mediates a transcription-dependent mechanism, which induces degradation of PGHS-2 mRNA.
USF phosphorylation has a role in the regulation of the PGHS-2 promoter in granulosa cells
The results are consistent with the hypothesis that arachidonic acid acts via PPARalpha to increase PTGS2 levels in bovine endometrial stromal cells.
COX-2 and FP receptor contribute via changes in amount and distribution to mechanisms associated with parturition.
The results demonstrate a pathway to the induction of COX-2 by PUFAs requiring NF-kappaB but not PPAR or PKC.
fibronectin fragment induced iNOS and COX-2 expression is downregulated in chondrocyte/agarose constructs
This study showed that COX-1 and COX-2 in genital carcinomas in the horse is poor; microsomal PGES-1 is more prominently expressed.
Progestin treatment does not affect expression of cytokines, steroid receptors, oxytocin receptor, and cyclooxygenase 2 in fetal membranes and endometrium.
mRNA transcription of prostaglandin synthases and their products in the equine endometrium in the course of fibrosis.
COX-1 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 mitogen-activated kinase (MAPK) in the signaling mechanism regulating pro-inflammatory cyclooxygenase (COX) gene expression in lipopolysaccharide (LPS)-activated equine leukocytes in horses is reported.
The effects of semen extender and seminal plasma on the expression of inflammatory modulators in the endometrium of mares are reported.
In this study, both COX-1 and COX-2 were expressed in the colon before induced ischemia; ischemic injury increased expression of COX-2.
Immunoreactivity for COX-1 and COX-2 is high in equine corneal SCC, possibly indicating that COX plays a role in oncogenesis or progression of this tumor type at this site.
immunoreactivity in equine ocular squamous-cell carcinoma
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 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.
Luteinizing hormone signaling induced ptgs2a expression is required for ovulation in zebrafish.
Mutations in the APC gene resultt in impaired retinoic acid biosynthesis and upegulation of cox2.
Retinoic acid inhibits beta-catenin through suppression of Cox-2
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
, prostaglandin-endoperoxide synthase 2