anti-F2RL2 (F2RL2) Antikörper

Human Coagulation Factor II (thrombin) Receptor-Like 2 (F2RL2) Interaktionspartner

1. PAR3 is essential in thrombin stimulated insulin secretion.

2. TFRGAP, a PAR-3 mimicking peptide significantly induced the phosphorylation of eNOS-Thr-495 with minimal phosphorylation of eNOS-Ser-1177 with no change in nitric oxide production.

3. These data provide intriguing novel insights into the diversification of functional selectivity of protease signaling achievable by canonical and noncanonical PAR activation, such as the activation of vascular-protective Tie2 by noncanonical PAR3 activation.

4. In pancreatic adenocarcinoma cells, PAR3 knockdown enhances cell adhesion. We propose this is due to increased expression of E-cadherin, leading to a greater adhesion of free-floating cells to cells bound to the surface via integrins, particularly ITGalphav.

5. Data indicate that knockdowns of all three PARs PAR-1, PAR-2, and PAR-3 exhibited changes in the expression of CDC42, which correlated with the changes in their invasion.

6. Elevated expression of PAR-3, but not PAR-4, was detected in the lungs of idiopathic pulmonary fibrosis patients.

7. A unique contributory role for PAR3 in the complex mechanisms underlying Activated protein C cytoprotective effects.

8. PAR-3 receptors interact with thrombin and increase heme oxygenase-1 expression in synovial fibroblasts.

9. Human PAR-3 is regulated post-transcriptionally via the mRNA-stabilizing factor HuR, whereas transcriptional control involves nuclear factor of activated T cells (NFAT).

10. FXa bound in a punctate manner to thrombi under shear, while thrombin and fibrin(ogen) distributed ubiquitously over platelet-fibrin thrombi

11. genetic polymorphism is associated with peripheral arterial disease severity

12. Low concentrations of alpha-thrombin accelerate tissue factor-induced thrombin generation on the surface of vascular smooth muscle cells, and this effect is mediated by PAR-3 and PAR-4.

13. Human cytomegalovirus induces PARs expression through transcriptional activation in endothelial cells, increasing sensitivity to thrombin.

14. A novel role is identified for PAR3 in thrombin signaling.

15. Down-regulation of connexin and par-3 signals early anaplasia and malignant change in rectal cancer.

16. upregulated thrombin generation and inhibition of fibrinolysis, occurred in one-third of the Stem cell transplant patients associating with the development of Graft versus host disease

17. Lower plasma levels of thrombin-antithrombin complex correlate to higher recanalisation rates after ischaemic stroke

18. differentiation of human monocytes is associated with differential expression of functionally active PARs that mediate distinct regulatory functions in inflammation and atherogenesis.

19. findings support a role for PAR1, and potentially PAR2 and PAR3 in the invasive phase of human placentation

20. PAR-3 is expressed in human SMC and triggers intracellular calcium signaling.

Mouse (Murine) Coagulation Factor II (thrombin) Receptor-Like 2 (F2RL2) Interaktionspartner

1. Data show that activated protein C signals via protease activated receptors PAR2/PAR3 to expand Treg cells, mitigating the disease in mice.

2. found a hypomethylated region mapping to Iqgap2 (IQ motif-containing GTPase activating protein 2) and F2rl2

3. Simultaneous depletion of PAR-1 and PAR-3 almost completely inhibited epithelial-mesenchymal transition in bleomycin-induced lung fibrosis.

4. these data point to a novel kallikrein 6 -signaling axis in neurons that is mediated by PAR1 and PAR2 and is positioned to contribute to neurodegeneration

5. Par3(-/-) mice were protected against ferric chloride-induced thrombosis of mesenteric arterioles and against thromboplastin-induced pulmonary embolism (protease-activated receptor-3 (PAR3)

6. PAR3 receptors and analogues can mediate cell signaling by interaction with PAR1-type thrombin receptors

7. Crystal structures reveal the molecular basis of the cofactor function of cleaved PAR3, bound to exosite I, on recognition of PAR4 by the active site of thrombin.