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High levels of high-sensitive C-reactive protein (show CRP Proteins) 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 (show IL1B Proteins) rs16944, IL1R2 (show IL1R2 Proteins) rs2071008, PLA2G7 rs9395208, FAM5C rs12732361, CD40 (show CD40 Proteins) rs1800686, and CD36 (show CD36 Proteins) rs2065666 were associated with coronary heart disease (CHD (show CHDH Proteins)), suggesting an important role of inflammation in the risk of CHD (show CHDH Proteins).
LpPLA2 is found in both LDL and HDL (show HSD11B1 Proteins) and is distributed differently in men with T1D without any relationship to CAC (show CA2 Proteins) 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/mTOR signaling pathway in human THP1 macrophages.
Plasma Lp-PLA2 concentration was independently associated with coronary heart disease in Chinese patients.
The distribution of V279F-AA+AC genotype and R92H-AA+AG genotype in the AP group was higher than that in the control group, whereas the Severity of Acute Pancreatitis (SAP (show APCS Proteins)) group and SAP (show APCS Proteins) with multiple organ dysfunction syndrome group distributions were higher than those in the MAP group and SAP (show APCS Proteins) without MODS group.G-C-A, G-A-G, and G-C-G haploids formed by A379V, V279F, and R92H may be associated with AP susceptibility
Lp-PLA2 augments the inflammatory response after MI and antagonizes healing by disrupting the balance between inflammation and repair.
Plg (show PLG Proteins) from mouse plasma contains oxPtdPC adducts that are not affected by the action of Lp-PLA(2), suggesting that linkage to Plg (show PLG Proteins) protects oxPtdPCs from metabolism during their transport in the plasma.
SAA (show SAA1 Proteins) up-regulates Lp-PLA2 production significantly via a FPRL1 (show FPR2 Proteins)/MAPKs./PPAR-gamma (show PPARG Proteins) signaling pathway.
Deletion of Pla2g7 decreases small intestinal polyp and colon tumor incidence in ApcMin/+ mice.
Macrophage VLDL receptor (show VLDLR Proteins) promotes PAFAH (show PAFAH1B1 Proteins) secretion in mother's milk and suppresses systemic inflammation in nursing neonates.
Pla2g7 and Tnfrsf21 (show TNFRSF21 Proteins) 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 (show NFE2L3 Proteins) and Pla2g7 are essential.
The effects of a specific lp-PLA2 inhibitor on atherosclerosis in ApoE (show APOE Proteins)-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 (show MMP9 Proteins), CCL2 (show CCL2 Proteins) 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