Browse our anti-P2RY1 (P2RY1) Antibodies

Mouse (Murine) Purinergic Receptor P2Y, G-Protein Coupled, 1 (P2RY1) interaction partners

1. 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

2. 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

3. This study demonstrated that The inhibitory input to mouse cerebellar Purkinje cells is reciprocally modulated by Bergmann glial P2Y1 and AMPA receptor signaling.

4. 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.

5. 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.

6. In the brain samples, expressions of P2Y4 and P2X7 were significantly reduced, whereas that of P2Y1 was significantly elevated in an age-dependent manner.

7. 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.

8. 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.

9. 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.

10. 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.

11. Antibody EL2Ab binds to and exhibits P2Y1R-dependent function-blocking activity in the context of platelets.

12. 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.

13. P2Y1 couples to and activates TRPV4. PKC inhibitors prevented P2Y1 receptor activation of TRPV4.

14. 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.

15. The analysis of single and double KO mice demonstrated that NTPDase2 and P2Y1 receptors are not required for murine eye formation

16. Data indicate that knock down of purinergic P2Y1 receptors inhibited directed migration in neurospheres.

17. In a mouse model of Alzheimer disease, astroglial network dysfunction is mediated by P2Y1 receptor signalling in reactive astrocytes.

18. 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.

19. This study shows that Up4A is a potent native agonist for P2Y1R and SK-channel activation in human and mouse colon.

20. RhoA signaling downstream of platelet P2Y, but not P2Y, represents a clear dichotomy in platelet activation during allergic inflammation versus hemostasis.

Guinea Pig Purinergic Receptor P2Y, G-Protein Coupled, 1 (P2RY1) interaction partners

1. P2Y1R activation at the plasma membrane inhibits direct activation of the inositol trisphosphate receptor in the sarcoplasmic reticulum.

Human Purinergic Receptor P2Y, G-Protein Coupled, 1 (P2RY1) interaction partners

1. high-risk gene-gene interactions among TXA2R rs1131882, P2Y1 rs1371097 and GPIIIa rs2317676 were associated with higher platelet activation, and independently associated with higher risk of carotid stenosis in ischemic stroke patients.

2. Genomic association study identified deleterious rare variants in P2RY1 in patients with ischemic stroke.

3. Pin1 induces the ADP-induced migration of human dental pulp cells through P2Y1 stabilization.

4. predominant role of P2Y1 receptors in human embryonic stem cells and a transition of P2Y-IP3R coupling in derived cardiovascular progenitor cells are responsible for the differential Ca(2+) mobilization between these cells.

5. The negative feedback modulation between LncRNA-SARCC/AR complex and HIF-2alpha signaling may then lead to differentially modulated RCC progression in a VHL-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/C-MYC signals against RCC progression.

6. these data highlight a key role of the P2Y1/PI3Kbeta axis in endothelial cell proliferation downstream of ecto-F1-ATPase activation by apoA-I. Pharmacological targeting of this pathway could represent a promising approach to enhance vascular endothelial protection.

7. ALIX regulates P2Y1 degradation.

8. There is increased expression of P2Y1 receptors in the rectosigmoid mucosa of diarrhea-predominant irritable bowel syndrome patients.

9. High extracellular NaCl induces priming of the NLRP3 inflammasome in RPE cells, in part via P2Y1 receptor signaling

10. aim of this study was to evaluate the effects of platelet receptor gene (P2Y12, P2Y1) and glycoprotein gene (GPIIIa) polymorphisms, as well as their interactions, on antiplatelet drug responsiveness and clinical outcomes in patients with acute MIS

11. Early neurological deterioration (END) occurred significantly more frequently in patients with aspirin resistance (AR) or high-risk interactive genotypes. Moreover, AR and high-risk interactive genotypes were independently associated with END.

12. Synergistic inhibition of both P2Y1 and P2Y12 adenosine diphosphate receptors by GLS-409 immediately attenuates platelet-mediated thrombosis and effectively blocks agonist-stimulated platelet aggregation irrespective of concomitant aspirin therapy.

13. Antibody EL2Ab binds to and exhibits P2Y1R-dependent function-blocking activity in the context of platelets.

14. P2Y1 couples to and activates TRPV4. PKC inhibitors prevented P2Y1 receptor activation of TRPV4.

15. P2Y1 receptors are a potential pharmacological target leading smooth muscle relaxation to treat spasticity in colonic motor disorders.

16. crystal structures of the human P2Y1R in complex with a nucleotide antagonist MRS2500 at 2.7 A resolution, and with a non-nucleotide antagonist BPTU at 2.2 A resolution

17. Data indicate that ATP-evoked Hoechst 33258 uptake was dependent on activation of P2Y receptors P2Y1 and P2Y2.

18. This study shows that Up4A is a potent native agonist for P2Y1R and SK-channel activation in human and mouse colon.

19. These studies demonstrate a role for P2Y receptor activation in stimulation of ATP release.

20. The immunohistochemical results were reflected in the immunoblotting data P2RY1 receptors were detected at higher levels of expression in patient with cortical dysplasia with intractable epilepsy.

Cow (Bovine) Purinergic Receptor P2Y, G-Protein Coupled, 1 (P2RY1) interaction partners

1. P2Y1 receptor-mediated responses involve Flt3 transactivation, and may identify a unique mechanism whereby cancer chemotherapy with receptor tyrosine kinase inhibitors promotes vascular dysfunction.

2. Purinergic P2Y1 receptor signaling mediates wound stimuli-induced cyclooxygenase-2 expression in intestinal subepithelial myofibroblasts.

3. P2Y1 and P2Y13 receptors play a major role in vasa vasorum endothelial cells growth responses.