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he PAFR gene rs5938 or rs313152 polymorphisms might be a potential biomarker for susceptibility to coronary heart disease.
Weighted gene co-expression network analysis of gene modules for the prognosis of esophageal cancer yielded PTAFR and FGR as the most important hub genes for predicting patient survival.
we demonstrate that PAFR inhibition can selectively enhances the sensitivity of radiotherapy in prostate cancer cells with elevated PAFR expression after irradiation exposure
PAFR overexpression is associated with pneumococcal infection.
WEB-2086 represents an innovative class of candidate drugs for inhibiting PAFr-dependent lung infections caused by the main bacterial drivers of smoking-related COPD.
PAF stimulation dose-dependently promoted the invasion, migration and growth of prostate cancer cells in vitro, while knockdow our findings demonstrate that PAFR can activate ERK1/2 pathway, and subsequently increase MMP-3 expression and decrease E-cadherin expression
PAFR is overexpressed in NSCLC as well as in breast, colorectal, and gastric carcinomas. PAFR expression correlates with clinical stages, survival time, and distant metastasis. PAF/PAFR signaling also upregulated IL6 expression and STAT3 activation.
we made the first demonstration that dysregulation of PAFR and the positive regulatory loop between PAFR and pAKT contribute to malignant progression of esophageal squamous cell carcinoma
Data support an important role for PAFR in tumor growth and suggest that engagement of PAFR interferes with selected pathways in macrophages, changing their phenotype into that of a regulatory with suppressor activities. [review]
Epithelial PAFr expression is upregulated in smokers, especially in those with COPD, and is not obviously affected by inhaled corticosteroid therapy.
Results suggest that WEB2086 and AG1478 are synergistic in ovarian cancer cells with high expression of both platelet-activating factor receptor (PAFR) and epidermal growth factor receptor (EGFR).
PAFR may have an important role in modulating the cisplatin sensitivity of ovarian cancer cells.
patients presenting elevated PAFR expression had significantly longer survival times compared to those with low PAFR expression (log-rank test, p<0.001).
oxLDL induces the recruitment of PAFR and CD36 into the same lipid rafts, which is important for oxLDL uptake and IL-10 production
Data suggest PAF/PAF receptor signaling exerts proinflammatory effect on neutrophil via down-regulation of LXRa (liver X receptor alpha) and target genes (ATP-binding cassette transporter (ABC) A1, ABC G1, sterol response element binding protein 1c).
Inhibition of platelet aggregation by lipoteichoic acid was blocked using a monoclonal anti-PafR antibody and Ginkgolide B,a well-defined PafR antagonist, demonstrating that the LTA inhibitory signal occurs via PafR.
oxLDL induces alternative macrophage activation by mechanisms involving CD36 and PAFR
Data suggest that expression of PAFR and SIRT1 (sirtuin 1) is down-regulated in endothelial progenitor cells of type 2 diabetic patients with poor glycaemic control compared to those with good glycaemic control.
An implication of platelet-activating factor receptor A224D mutation in the susceptibility to relapsing-remitting multiple sclerosis in Tunisian population.
recognition of apoptotic cells by phagocytes leads to activation of PAFR pathways, resulting in a microenvironment response favorable to melanoma growth
PAF and luteinizing hormone signaling plays an important role in regulating the production of excessive oxidants.
The results provide clear evidence for expression of PAFr in bovine granulosa cells and its functional involvement in PAF/PAFr-mediated stimulation of cell recruitment.
Our results thus define a key inflammatory molecule PAF that participates in the neuroinflammation and helps bring about cerebral dysfunction during the TBI acute phase.
PAFR role in modulating activation of NF-kappaB and in the pro- and anti-inflammatory responses during toll-like receptor activation in in macrophages.
this study shows that tumors grew less in PAFR KO mice
The findings above were confirmed in lipopolysaccharide (LPS)-incubated cardiomyocytes with or without PAFR expressions in vitro. In summary, we supposed that inhibiting PAFR reduced inflammation, oxidative stress and apoptosis, and thus might be a promising therapeutic strategy to alleviate myocardial I/R injury.
PAFR null mutant mice showed a better functional recovery in grip and rotarod performances than wild-type mice.
Results show that CD36 and Platelet-Activating Factor Receptor are important mediators of house dust mites (HDM) allergy development and that inhibiting HDM engagement with phosphorylcholine receptors in the lung protects against allergic airway disease.
Study demonstrated that PAFR has a compelling involvement in Brucella abortus uptake as a promoter of phagocytosis, which is associated with JAK2 signaling activation.
In the absence of PAFR signalling, monocytes and macrophages acquire a pro-inflammatory phenotype, resulting in adipose tissue inflammation and metabolic dysfunction.
Data (including data from studies in knockout mice) suggest that signal transduction via platelet-activating factor (PAF) and PAF receptor is involved in regulation of lipid metabolism/inflammation in liver of mice on high-refined carbohydrate diet.
ExoU activates NF-kappaB by PAFR signalling, which in turns enhances PAFR expression, highlighting an important mechanism of amplification of response to this P. aeruginosa toxin.
In PAF receptor-knockout mice, diet-induced obesity is exacerbated.
Bacteria did not associate with PAFR, indicating an indirect role of PAFR in pneumococcal adhesion to endothelial cells.
PAFR deficiency resulted in less inflammation in adipose tissue and improvement in glucose homeostasis in mice fed a high-carbohydrate diet
PAFR and CD36 coimmunoprecipitated with flotillin-1, a constitutive lipid raft protein, and disruption of these membrane microdomains by methyl-beta-cyclodextrin reduced apoptotic cells phagocytosis
Our findings establish the existence of a functional partnership PAF-R/eNOS on endothelial cell plasma membrane.
Activation of PAF-receptor induces regulatory dendritic cells through PGE2 and IL-10.
PAFR signaling contributes to a pro-inflammatory environment in the model of obstructive nephropathy, favoring the fibrotic process.
propose for the first time that PAF/PAF-R can mediate dopaminergic degeneration via an NF-kappaB-dependent signaling process
EfLTA induces the expression of chemokines via signaling pathways requiring TLR2 and PAFR, which is distinct from that of LPS-induced chemokine expression.
Blockade of platelet-activating factor receptor may contribute to the progression of periodontal disease triggered by Aggregatibacter actinomycetemcomitans by directly affecting the differentiation and activity of osteoclasts.
The gene expression of PAFR was upregulated, as an effect of light exposure, in the third eyelid but not in the cornea.
This gene encodes a seven-transmembrane G-protein-coupled receptor for platelet-activating factor (PAF) that localizes to lipid rafts and/or caveolae in the cell membrane. PAF (1-0-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine) is a phospholipid that plays a significant role in oncogenic transformation, tumor growth, angiogenesis, metastasis, and pro-inflammatory processes. Binding of PAF to the PAF-receptor (PAFR) stimulates numerous signal transduction pathways including phospholipase C, D, A2, mitogen-activated protein kinases (MAPKs), and the phosphatidylinositol-calcium second messenger system. Following PAFR activation, cells become rapidly desensitized and this refractory state is dependent on PAFR phosphorylation, internalization, and down-regulation. Alternative splicing results in multiple transcript variants.
, platelet-activating factor receptor
, PAF receptor