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We found that overexpression of P2Y1 receptors in astrocytes did not increase microdomain Ca(2+) signals in astrocyte processes but caused Ca(2+) wavelike signals
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upregulation of P2Y1 in cutaneous nociceptors during early life peripheral inflammation can regulate the sensitization of myelinated nociceptors to both mechanical and heat stimuli possibly through modulation of transient receptor potential vanilloid type 1 expression
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This study demonstrated that The inhibitory input to mouse cerebellar Purkinje cells is reciprocally modulated by Bergmann glial P2Y1 and AMPA receptor signaling.
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LPS-induced inflammation levels were comparable in the P2Y1-null and wild-type mice. Specifically, splenomegaly, counts of circulating platelets and white blood cells (lymphocytes and neutrophils), and assessments of lung injury (tissue architecture and cell infiltration) were similar in the P2Y1-null and wild-type mice. I conclude that lung injury during LPS-induced inflammation in mice is independent of P2Y1 signaling.
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In P2Y12(-/-) mice, the growth of syngeneic ovarian cancer tumors was reduced by >85% compared with wild-type (WT) mice. In contrast, there was no difference in tumor growth between P2Y1(-/-) and WT mice.
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In the brain samples, expressions of P2Y4 and P2X7 were significantly reduced, whereas that of P2Y1 was significantly elevated in an age-dependent manner.
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Mesenteric endothelial cells are primed by schistosomiasis to a pro-inflammatory phenotype characterized by an increased expression of NTPDases 2 and 3, favoring ADP accumulation and mononuclear cell adhesion, possibly contributing to mesenteric inflammation and schistosomiasis morbidity via P2Y1 receptor signaling.
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the amounts of AChE activity, AChE catalytic subunit, structure subunit PRiMA and the amount of acetylcholine, in the brain were not, significantly, altered, suggesting the role of P2Y1R in neuron could have different function as that in muscle.
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In P2Y1R (-/-) mice, the expression of P2Y2 receptor in muscle was reduced by over 50 %, as compared to P2Y1R (+/+) mice. P2Y1 receptor regulated the neuromuscular junction gene expression.
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Our current results suggest that P2Y1 modulates heat responsiveness and chemosensation in muscle afferents to play a key role in the development of pain-related behaviors during ischemia.
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Antibody EL2Ab binds to and exhibits P2Y1R-dependent function-blocking activity in the context of platelets.
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Provide evidence for purinergic glio-endothelial coupling during neuronal activity, highlighting the role of ATP-mediated activation of eNOS via P2Y1 receptors in functional hyperemia.
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P2Y1 couples to and activates TRPV4. PKC inhibitors prevented P2Y1 receptor activation of TRPV4.
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The results of this study indicated that activation of the P2Y1R stimulates fibre growth and thereby emphasises the general role of this particular receptor subtype during development and regeneration.
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The analysis of single and double KO mice demonstrated that NTPDase2 and P2Y1 receptors are not required for murine eye formation
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Data indicate that knock down of purinergic P2Y1 receptors inhibited directed migration in neurospheres.
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In a mouse model of Alzheimer disease, astroglial network dysfunction is mediated by P2Y1 receptor signalling in reactive astrocytes.
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P2Y1R-KO mice displayed reduced cell numbers in the ganglion cell and inner nuclear layers, ischemia induced apoptotic death of cells in all retinal layers.
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This study shows that Up4A is a potent native agonist for P2Y1R and SK-channel activation in human and mouse colon.
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RhoA signaling downstream of platelet P2Y, but not P2Y, represents a clear dichotomy in platelet activation during allergic inflammation versus hemostasis.
