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anti-Mouse (Murine) PLA2G5 Anticorps:
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Cow (Bovine) Polyclonal PLA2G5 Primary Antibody pour WB - ABIN2776806
Wootton, Arora, Drenos, Thompson, Cooper, Stephens, Hurel, Hurt-Camejo, Wiklund, Humphries, Talmud: Tagging SNP haplotype analysis of the secretory PLA2-V gene, PLA2G5, shows strong association with LDL and oxLDL levels, suggesting functional distinction from sPLA2-IIA: results from the UDACS study. dans Human molecular genetics 2007
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macrophage-associated Pla2g5 contributes significantly to type-2 immunity through regulation of IL-33 induction and free fatty acids-driven group 2 innate lymphoid cell activation
Deficiency of GV sPLA2 results in diminished glucose-stimulated insulin secretion in isolated pancreatic beta-cells
GV sPLA2 is involved in the maintenance of tubular cell function and integrity, promoting sodium retention through increased cortical (Na+ + K+)-ATPase expression and activity.
AdPLA2 plays an important role in promoting tumorigenesis and disease progression by modulating the production of prostaglandins and may serve as a potential therapeutic target in TSC and LAM.
PLA2G5 hydrolyzed phosphatidylcholine in fat-overladen low-density lipoprotein to release unsaturated fatty acids, which prevented palmitate-induced M1 macrophage polarization.
Key Data shows the role of group v secreted phospholipase A2 in Th2 cytokine and dendritic cell-driven airway hyperresponsiveness and remodeling.
Our studies identified a unique function of gV-sPLA2 in activation of macrophages
The impact of group V sPLA(2) deficiency on angiotensin (Ang) II-induced cardiac fibrosis in apoE deficient mice was investigated.
The results indicate that the PLA(2) activity also plays a substantial role in protecting cells against oxidant stress caused by an exogenous hydroperoxide.
GV sPLA(2) in bone marrow-derived myeloid cells as well as non-myeloid cells, which are likely bronchial epithelial cells, participate in the regulation of the innate immune response to pulmonary infection with E. coli.
Data from cuprizone-induced model of multiple sclerosis suggest that sPLA2 down-regulation during remyelination can limit release of AA and consequent production of pro-inflammatory PGs/TXB2 (which are increased during demyelination).
sPLA(2)-V plays an important role in the pathogenesis of myocardial ischemia reperfusion injury partly in concert with the activation of cPLA(2)
agonist-induced MAPK activation leads to Prdx6 phosphorylation and translocation to the cell membrane, where its PLA(2) activity facilitates assembly of the NOX2 complex and activation of the oxidase.
expression of group V sPLA(2) in antigen-presenting cells regulates Ag processing and maturation of dendritc cells and contributes to pulmonary inflammation and immune response against D. farinae.
J-774 cells incubated with Group V secretory phospholipase A(2) hydrolyzed-LDL produced more TNF-alpha and IL-6 compared to cells incubated with control-LDL.
Demonstrate the role of sPLA(2)-V in lipopolysaccharide-induced ICAM-1 and VCAM-1 protein overexpression and leukocyte recruitment, supporting the contribution of sPLA(2)-V in the development of inflammatory innate immune responses.
the effect of group IIa and V PLA2s on H2O2-induced AA release is dependent upon the presence of cPLA2alpha and the activation of PKC and ERK1/2. Group IIa and V PLA2s are regulatory and cPLA2alpha is responsible for AA release.
encapsulation of Group V PLA2 into granules brings the enzyme to the perinuclear envelope during cell activation
a role in innate immunity.
GIVA PLA2 is the dominant player involved in AA release, but it appears not to be involved in the regulation of LPS-induced expression of GV PLA2 or cyclooxygenase-2
This report provides the first demonstration that Phosphatidylcholine-Isoprostanes are readily hydrolyzed by group IIA, V and X Secretory Phospholipases A2.
Low GV-PLA2 expression is associated with cancer.
Data show that phospholipase A2 group IIA, V and X have different target/function related activity.
The clinical findings in this family suggest a diagnosis of benign familial fleck retina with excellent prognosis, in which the PLA2G5 gene may play a role.
sPLA2-V plays a thrombogenic role by impairing the ability of EPCR to promote protein C activation.
results demonstrate that EPCR is overexpressed and mediates the aggressive behavior of rheumatoid synovial fibroblasts, and is likely driven by group V secretory phospholipase A2
expression of PLA2s-IIE and -V correlates with the development of calcification as well as the expression of pro-osteogenic molecules in human aortic valves
Summarizing, Der p1 and Fel d1 involve phospholipase A2 enzymes in their action.
There is no association between rs525380 polymorphism of PLA2G5 and coronary heart disease.
Our results demonstrate the association of the PLA2G5 rs11573191 polymorphism with premature CAD. In our study, it was possible to distinguish one haplotype associated with increased risk of premature CAD and hypertension.
Human group V secretory phospholipase A2 is associated with lipid rafts and internalized in a flotillindependent pathway.
The effects of acidic pH on the activity of recombinant human group V secreted phospholipase A(2) (sPLA(2)-V) toward small VLDL (sVLDL), IDL, and LDL, on the binding of these apoB-100-containing lipoproteins to human aortic proteoglycans, were examined.
Biallelic mutations in PLA2G5, encoding group V phospholipase A2, cause benign fleck retina
Group V phospholipase A2 mediates barrier disruption of human pulmonary endothelial cells caused by LPS in vitro
circulating human neutrophils express groups V and X sPLA(2) (GV and GX sPLA(2)) mRNA and contain GV and GX sPLA(2) proteins, whereas GIB, GIIA, GIID, GIIE, GIIF, GIII, and GXII sPLA(2)s are undetectable
PLA2G5 binds to PLA2G4 to induce leukotriene synthesis in neutrophils
stimulation of three isoforms of PLA2 by thapsigargin liberates free AA that, in turn, induces capacitative calcium influx in human T-cells
group V phospholipase A2 induces group IVA phospholipase A2-independent cysteinyl leukotriene synthesis in human eosinophils
sPLA2-V expression in hepatocytes is induced by viral infection, fibrosis, and circulatory disturbance. Immunostaining using sPLA2-V antibody is useful for the detection of injured hepatocytes in patients with liver diseases.
This gene is a member of the secretory phospholipase A2 family. It is located in a tightly-linked cluster of secretory phospholipase A2 genes on chromosome 1. The encoded enzyme catalyzes the hydrolysis of membrane phospholipids to generate lysophospholipids and free fatty acids including arachidonic acid. It preferentially hydrolyzes linoleoyl-containing phosphatidylcholine substrates. Secretion of this enzyme is thought to induce inflammatory responses in neighboring cells. Alternatively spliced transcript variants have been found, but their full-length nature has not been determined.
calcium-dependent phospholipase A2
, phospholipase A2, group V
, group V phospholipase A2
, phosphatidylcholine 2-acylhydrolase 5
, Ca2+-dependent phospholipase A2
, phospholipase A2, group 5