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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 (show GRIA3 ELISA Kits) receptor signaling.
LPS (show TLR4 ELISA Kits)-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 (show TLR4 ELISA Kits)-induced inflammation in mice is independent of P2Y1 signaling.
In P2Y12 (show P2RY12 ELISA Kits)(-/-) 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.
In the brain samples, expressions of P2Y4 (show P2RY4 ELISA Kits) and P2X7 (show P2RX7 ELISA Kits) were significantly reduced, whereas that of P2Y1 was significantly elevated in an age-dependent manner.
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.
the amounts of AChE activity, AChE catalytic subunit, structure subunit PRiMA (show PRIMA1 ELISA Kits) 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.
In P2Y1R (-/-) mice, the expression of P2Y2 (show P2RY2 ELISA Kits) receptor in muscle was reduced by over 50 %, as compared to P2Y1R (+/+) mice. P2Y1 receptor regulated the neuromuscular junction gene expression.
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.
Provide evidence for purinergic glio-endothelial coupling during neuronal activity, highlighting the role of ATP-mediated activation of eNOS (show NOS3 ELISA Kits) via P2Y1 receptors in functional hyperemia.
P2Y1 couples to and activates TRPV4 (show TRPV4 ELISA Kits). PKC (show PKC ELISA Kits) inhibitors prevented P2Y1 receptor activation of TRPV4 (show TRPV4 ELISA Kits).
predominant role of P2Y1 receptors in human embryonic stem cells and a transition of P2Y-IP3R (show ITPR1 ELISA Kits) coupling in derived cardiovascular progenitor cells are responsible for the differential Ca(2 (show CA2 ELISA Kits)+) mobilization between these cells.
The negative feedback modulation between LncRNA-SARCC/AR complex and HIF-2alpha (show EPAS1 ELISA Kits) signaling may then lead to differentially modulated RCC (show XRCC1 ELISA Kits) progression in a VHL (show VHL ELISA Kits)-dependent manner. Together, these results may provide us a new therapeutic approach via targeting this newly identified signal from LncRNA-SARCC to AR-mediated HIF-2alpha (show EPAS1 ELISA Kits)/C-MYC (show MYC ELISA Kits) signals against RCC (show XRCC1 ELISA Kits) progression.
these data highlight a key role of the P2Y1/PI3Kbeta axis in endothelial cell proliferation downstream of ecto (show TRIM33 ELISA Kits)-F1-ATPase (show DNAH8 ELISA Kits) activation by apoA-I (show APOA1 ELISA Kits). Pharmacological targeting of this pathway could represent a promising approach to enhance vascular endothelial protection.
ALIX (show PDCD6IP ELISA Kits) regulates P2Y1 degradation.
There is increased expression of P2Y1 receptors in the rectosigmoid mucosa of diarrhea-predominant irritable bowel syndrome patients.
High extracellular NaCl induces priming of the NLRP3 (show NLRP3 ELISA Kits) inflammasome in RPE cells, in part via P2Y1 receptor signaling
aim of this study was to evaluate the effects of platelet receptor gene (P2Y12 (show P2RY12 ELISA Kits), P2Y1) and glycoprotein gene (GPIIIa (show ITGB3 ELISA Kits)) polymorphisms, as well as their interactions, on antiplatelet drug responsiveness and clinical outcomes in patients with acute MIS (show AMH ELISA Kits)
Synergistic inhibition of both P2Y1 and P2Y12 (show P2RY12 ELISA Kits) adenosine diphosphate receptors by GLS (show GLS ELISA Kits)-409 immediately attenuates platelet-mediated thrombosis and effectively blocks agonist-stimulated platelet aggregation irrespective of concomitant aspirin therapy.
P2Y1 couples to and activates TRPV4 (show TRPV4 ELISA Kits). PKC inhibitors prevented P2Y1 receptor activation of TRPV4 (show TRPV4 ELISA Kits).
P2Y1 receptors are a potential pharmacological target leading smooth muscle relaxation to treat spasticity in colonic motor disorders.
P2Y1 receptor-mediated responses involve Flt3 (show FLT3 ELISA Kits) transactivation, and may identify a unique mechanism whereby cancer chemotherapy with receptor tyrosine kinase (show RET ELISA Kits) inhibitors promotes vascular dysfunction.
Purinergic P2Y1 receptor signaling mediates wound stimuli-induced cyclooxygenase-2 (show PTGS2 ELISA Kits) expression in intestinal subepithelial myofibroblasts.
P2Y1 and P2Y13 (show P2RY13 ELISA Kits) receptors play a major role in vasa (show DDX4 ELISA Kits) vasorum endothelial cells growth responses.
The product of this gene belongs to the family of G-protein coupled receptors. This family has several receptor subtypes with different pharmacological selectivity, which overlaps in some cases, for various adenosine and uridine nucleotides. This receptor functions as a receptor for extracellular ATP and ADP. In platelets binding to ADP leads to mobilization of intracellular calcium ions via activation of phospholipase C, a change in platelet shape, and probably to platelet aggregation.
, P2Y purinoceptor 1
, P2Y1 receptor
, P2Y1 purinoceptor
, P2 purinoceptor subtype Y1
, platelet ADP receptor
, P2 purinoreceptor subclass 2Y
, P2Y ATP receptor 1
, ATP receptor P2Y1
, G protein-coupled receptor
, p2y1 purinoceptor