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Blockade of the P2X7 receptor reduces cyst formation via ERK (show MAPK1 Proteins)-dependent pathways in a zebrafish model of polycystic kidney disease.
that the P2X7R rs3751143 functional polymorphism might contribute to osteoporosis susceptibility in Chinese postmenopausal women
indicating the involvement of P2X7R in the growth of esophageal squamous cell carcinoma
Data show that Pr2x7 gene deletion protects from HFD-induced NASH (show SAMSN1 Proteins), possibly through blunted activation of NLRP3 (show NLRP3 Proteins) inflammasome.
this study demonstrates that P2X7 is not essential for development of imiquimod -induced psoriasis-like inflammation
This study revealed that the P2X7R/NLRP3 (show NLRP3 Proteins) pathway plays important roles in IL-1beta (show IL1B Proteins) secretion and inhibition of Toxoplasma gondii proliferation in small intestinal epithelial cells.
P2X7R contributes to the progression of spinal TB. The P2X7 -762C>T and 489C>T polymorphisms are correlated with susceptibility to spinal TB. Carrying the -762CC genotype and 489T allele increases the risk of developing spinal TB in a Southern Chinese Han population.
Increased expression of P2X7R in peripheral blood mononuclear cells from patients with rheumatoid arthritis.P2X7R role in th17 cells differentiation.
results show that P2X7 is a scavenger receptor with important function in the CNS but its phagocytic function has features distinct from its pore function. Both P2X7 pore formation and P2X7-mediated phagocytosis should be considered in the design of new P2X7 antagonists for the treatment of CNS diseases.
This pathway provides new insight into factors that increase dynamic blebbing and identifies new targets, such as P2X7, that can be used to improve the culture of cells with therapeutic potential.
a major role for P2X7R and P2Y11R in ATP-mediated inhibition of tumor-derived endothelial cell migration, is reported.
For the inflammasome-dependent IL-1beta (show IL1B Proteins) release, bovine monocytes require ATP in addition to a primary stimulus. This IL-1beta (show IL1B Proteins) release depends on potassium efflux, but, in contrast to human and murine monocytes, does not require calcium influx or generation of reaction oxygen and is independent of the P2X7 receptor.
Inhibition or knockout of P2X7 receptors attenuated surgery and anesthesia-induced neuroinflammation and cognitive impairment. We conclude that surgery under desflurane anesthesia may have reduced neuroinflammation and cognitive impairment compared with surgery under isoflurane anesthesia. P2X7 receptors may mediate the neuroinflammation and cognitive impairment after surgery.
Data show that Pr2x7 gene deletion protects from HFD-induced NASH (show SAMSN1 Proteins), possibly through blunted activation of NLRP3 (show NLRP3 Proteins) inflammasome
The results of this study suggested that specific pharmacological or genetic blockade of P2X7R promotes anxiogenic-like effects, along with deficits in extinction learning.
genetic ablation of the P2X7 receptor attenuated the IL-1beta (show IL1B Proteins) and IL-6 (show IL6 Proteins) production in the brain from septic mice. Furthermore, our results suggest a crucial role for the enzyme CD39 (show ENTPD1 Proteins) in limiting P2X7 receptor proinflammatory responses since CD39 (show ENTPD1 Proteins)(-/-) septic mice exhibited higher levels of IL-1beta (show IL1B Proteins) in the brain.
P2X7R role in th17 cells differentiation.
Studies indicate the role of P2X7R (purinergic 2X7 receptor) and NLRP3 (show NLRP3 Proteins) (NACHT, LRR, and PYD domains-containing protein 3 (show HSPB3 Proteins)) inflammasome activation in the process of pancreatic fibrosis in chronic pancreatitis (CP) and suggest that blockade of P2X7R-NLRP3 (show NLRP3 Proteins) inflammasome signaling pathway may represent a therapeutic strategy for CP and its fibrotic process.
CD39 (show ENTPD1 Proteins) expression in macrophages limits P2X7-mediated pro-inflammatory responses, scavenging extracellular ATP and ultimately generating adenosine. CD39 (show ENTPD1 Proteins) genetic deletion exacerbates sepsis-induced experimental liver injury.
P2X7 receptor signaling is involved in neuronal cell death after axonal injury, being P2X7 receptor antagonism a potential therapeutic strategy.
Results show P2xr7-dependent synaptic alterations in the learned helplessness animal model of depression, suggesting a potential structural correlate of the antidepressant effect of genetic deletion of P2rx7.
The product of this gene belongs to the family of purinoceptors for ATP. This receptor functions as a ligand-gated ion channel and is responsible for ATP-dependent lysis of macrophages through the formation of membrane pores permeable to large molecules. Activation of this nuclear receptor by ATP in the cytoplasm may be a mechanism by which cellular activity can be coupled to changes in gene expression. Multiple alternatively spliced variants have been identified, most of which fit nonsense-mediated decay (NMD) criteria.
P2X purinoceptor 7
, purinergic receptor P2X, ligand-gated ion channel, 7
, p2X purinoceptor 7-like
, ATP receptor
, P2X7 receptor
, P2Z receptor
, purinergic receptor P2X7 variant A
, P2X7 purinoceptor
, purinergic receptor P2X7