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Human Polyclonal Lp-PLA2 Primary Antibody pour IF (p), IHC (p) - ABIN686722
Rosing, Fobker, Kannenberg, Gunia, DellAquila, Kwiecien, Stypmann, Nofer: Everolimus therapy is associated with reduced lipoprotein-associated phospholipase A2 (Lp-Pla2) activity and oxidative stress in heart transplant recipients. dans Atherosclerosis 2013
Show all 2 Pubmed References
Human Polyclonal Lp-PLA2 Primary Antibody pour ELISA, WB - ABIN4238414
Moldoveanu, Serban, Marta, Serban, Huica: Lipoprotein-associated phospholipase A2 activity in patients with preserved left ventricular ejection fraction. dans Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals 2011
Human Monoclonal Lp-PLA2 Primary Antibody pour ELISA - ABIN563501
Klee, Finlay, McDonald, Attewell, Hebrink, Dyer, Love, Vasmatzis, Li, Beechem, Klee: Bioinformatics methods for prioritizing serum biomarker candidates. dans Clinical chemistry 2007
Human Polyclonal Lp-PLA2 Primary Antibody pour FACS, IHC (p) - ABIN653776
Bouchareb, Mahmut, Nsaibia, Boulanger, Dahou, Lépine, Laflamme, Hadji, Couture, Trahan, Pagé, Bossé, Pibarot, Scipione, Romagnuolo, Koschinsky, Arseneault, Marette, Mathieu: Autotaxin Derived From Lipoprotein(a) and Valve Interstitial Cells Promotes Inflammation and Mineralization of the Aortic Valve. dans Circulation 2015
The substitution of whole grains and legumes for refined rice resulted in a reduction in Lp-PLA2 activities in plasma and PBMCs partly through improved glycemic control, increased consumption of protein relative to carbohydrate, and reduced lipid peroxides.
High levels of high-sensitive C-reactive protein (Montrer CRP Anticorps) and lipoprotein-associated phospholipase-A2 did not relate to endothelial dysfunction in ST-elevation myocardial infarction patients treated with percutaneous coronary intervention.
In persistent prehypertension, increased ox-LDL hydrolysis by Lp-PLA2 enhances arterial stiffness without an age-related increase in blood pressure.
Data show that all the six inflammation-related CpG-SNPs genotypes including IL1B (Montrer IL1B Anticorps) rs16944, IL1R2 (Montrer IL1R2 Anticorps) rs2071008, PLA2G7 rs9395208, FAM5C rs12732361, CD40 (Montrer CD40 Anticorps) rs1800686, and CD36 (Montrer CD36 Anticorps) rs2065666 were associated with coronary heart disease (CHD (Montrer CHDH Anticorps)), suggesting an important role of inflammation in the risk of CHD (Montrer CHDH Anticorps).
LpPLA2 is found in both LDL and HDL (Montrer HSD11B1 Anticorps) and is distributed differently in men with T1D without any relationship to CAC (Montrer CA2 Anticorps) score progression
In a multi-ethnic cohort without baseline cardiovascular disease, higher Lp-PLA2 mass and activity were not significantly associated with an increased risk for incident peripheral arterial disease.
The simultaneous presence of the PLA2G7 279VV genotype and persistence of overweight synergistically increases the risk for hypertension.
Elevated mass and activity of Lp-PLA2 related to inflammation and atherosclerosis may take part in the development of kidney injury and atherosclerosis in patients with chronic kidney disease.
Taken together, these results revealed that Lp-PLA2 silencing protected against ox-LDL-induced oxidative stress and cell apoptosis via Akt (Montrer AKT1 Anticorps)/mTOR (Montrer FRAP1 Anticorps) signaling pathway in human THP1 (Montrer GLI2 Anticorps) macrophages.
Plasma Lp-PLA2 concentration was independently associated with coronary heart disease in Chinese patients.
Lp-PLA2 augments the inflammatory response after MI and antagonizes healing by disrupting the balance between inflammation and repair.
Plg (Montrer PLG Anticorps) from mouse plasma contains oxPtdPC adducts that are not affected by the action of Lp-PLA(2), suggesting that linkage to Plg (Montrer PLG Anticorps) protects oxPtdPCs from metabolism during their transport in the plasma.
SAA (Montrer SAA1 Anticorps) up-regulates Lp-PLA2 production significantly via a FPRL1 (Montrer FPR2 Anticorps)/MAPKs./PPAR-gamma (Montrer PPARG Anticorps) signaling pathway.
Deletion of Pla2g7 decreases small intestinal polyp and colon tumor incidence in ApcMin/+ mice.
Macrophage VLDL receptor (Montrer VLDLR Anticorps) promotes PAFAH (Montrer PAFAH1B1 Anticorps) secretion in mother's milk and suppresses systemic inflammation in nursing neonates.
Pla2g7 and Tnfrsf21 (Montrer TNFRSF21 Anticorps) have been identified as genetic susceptibility to influenza genes in mice.
Pla2g7 plays a crucial physiological role in smooth muscle cell differentiation from stem cells, and interactions between Nrf3 (Montrer NFE2L3 Anticorps) and Pla2g7 are essential.
The effects of a specific lp-PLA2 inhibitor on atherosclerosis in ApoE (Montrer APOE Anticorps)-deficient mice and its associated mechanisms, are reported.
Studies designed to evaluate the ability of precursor forms of PAF-AH to mature to fully active proteins indicated that the N-terminal end of human and mouse PAF-AH played important and opposite roles in this process.
PAF acetylhydrolase activity in the uterus in early pregnancy was not produced locally but probably resulted from the influx of the plasma form of the enzyme
The results demonstrated that Lp-PLA2 is associated with triglycerides which may be helpful for understanding the relationship of this protein with cardiovascular disease.
Effect of splenectomy and autologous spleen transplantation on the serum PAF-AH activity and acute-phase response in a porcine model are reported.
observations support a proatherogenic role for Lp-PLA2
Variable gene expression (eg, matrix metalloproteinase-9 (Montrer MMP9 Anticorps), CCL2 (Montrer CCL2 Anticorps) and Lp-PLA(2) mRNAs), both in regard to the arterial bed and duration of disease, was associated with variable plaque development and progression.
The significant correlation between PLA2G7 RNA expression in plaque macrophages and plasma PAFAH activity suggests that the latter is a consequence, rather than a cause of macrophage accumulation.
The protein encoded by this gene is a secreted enzyme that catalyzes the degradation of platelet-activating factor to biologically inactive products. Defects in this gene are a cause of platelet-activating factor acetylhydrolase deficiency. Two transcript variants encoding the same protein have been found for this gene.
, 2-acetyl-1-alkylglycerophosphocholine esterase
, LDL-associated phospholipase A2
, PAF 2-acylhydrolase
, PAF acetylhydrolase
, group-VIIA phospholipase A2
, lipoprotein-associated phospholipase A2
, platelet-activating factor acetylhydrolase
, group VII phospholipase A2
, plasma PAF acetylhydrolase