anti-F2R (F2R) Antikörper

Human Coagulation Factor II (thrombin) Receptor (F2R) Interaktionspartner

1. The activation of PAR-1 on the cell surface of SGC7901 and AGS cells was significantly reduced after the knockdown of EPCR. By contrast, blockade of PAR-1 reduced the proliferation and migration of gastric cells in vitro

2. Our structural data showed subtle changes in the binding pose between Vorapaxar and F16357. Transmembrane helices 1, 2, 5, and 7 were most significantly affected; most notably a large kink at F279(5.47) in TM helix 5 of the Vorapaxar complex was completely absent in the F16357 complex. The results of this study facilitate the future development of other therapeutic PAR1 antagonists.

3. Platelets were activated in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) patients, and such activation was at least partially attributed to the thrombin-protease-activated receptors (PARs) pathway.

4. Using protein C-factor VII chimera demonstrate that APC light chain amino acid residues outside the EPCR-binding site enable cytoprotective PAR1 signaling.

5. Study demonstrated that nerve activation by mucosal biopsy supernatants depends on proteases. This is a common feature of quiescent ulcerative colitis and irritable bowel syndrome (IBS) and may relate to some common gastrointestinal symptoms. However, only proteases in IBS supernatants signal through PAR1.

6. Data show there was no significant correlation of autoantibodies to coagulation factor II thrombin receptor (F2R; protease-activated receptor 1, PAR1) (PAR1-AB) level with , progression-free (PFS) and overall (OS) survival.

7. we found that activation of the protease-activated receptor 1 (PAR1) induced secretion of TSLP by the corneal stromal cells... we proposed that TSLP might function as the link between increased protease activity and inflammatory responses or itch sensation in the

8. PAR-1 in non-small-cell lung cancer is mainly expressed on cells that constitute the pulmonary tumor microenvironment, including vascular endothelial cells, macrophages and stromal fibroblasts.

9. thrombin binding to PAR-1 receptor activated Gi-protein/c-Src/Pyk2/EGFR/PI3K/Akt/p42/p44 MAPK cascade, which in turn elicited AP-1 activation and ultimately evoked MMP-9 expression and cell migration in SK-N-SH cells.

10. this study demonstrates that TGFbeta is a positive regulator of PAR-1 expression in A549 lung adenocarcinoma cells, which in turn increases the sensitivity of these cells to thrombin signalling

11. Taken together, these results indicated that PAR1 signalingmediated cJun activation promotes early apoptosis of HUVEC cells induced by heat stress.

12. The DHA - naringenin hybrid presented triple antiplatelet activity simultaneously targeting PAR-1, P2Y12 and COX-1 platelet activation pathways

13. Dabigatran increases platelet reactivity by enhancing the thrombin receptor density on platelets

14. Thrombin, via PAR1 activation, synergistically augments LPS-induced Human endometrial endothelial cells production of chemokines involved in immune cell recruitment and survival, suggesting a mechanism by which intrauterine abruption and bacterial infection may together be associated with an aggravated uterine inflammatory response.

15. EPCR occupancy recruits G-protein coupled receptor kinase 5, thereby inducing beta-arrestin-2 biased PAR1 signaling by both APC and thrombin. In

16. Data suggest that the abrogation of protease-activated receptor 1 (PAR1)-dependent signaling pathways may prove a promising strategy for gliomas.

17. these data indicate that KLKB1 induces inflammatory reactions in human dental tissues via protease-activated receptor 1

18. In this study, we found upregulation of several hemostasis-related genes, including the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-deleted MLL-AF9 cells. Similar to the effect of Runx1/Cbfb deletion, PAR-1 overexpression induced CDKN1A/p21 expression and attenuated proliferation in MLL-AF9 cells

19. Data highlight functional differences in proliferation and barrier integrity between dark keratinocytes and fair keratinocytes that are partly associated with their differential expression of PAR1 and PAR2.

20. the contribution of PAR1 and PAR4 to thrombin-mediated activation of the platelet fibrin receptor (GPIIbIIIa), is reported.

Mouse (Murine) Coagulation Factor II (thrombin) Receptor (F2R) Interaktionspartner

1. These results support the concept that APC-induced, PAR1-dependent biased signaling following R46 cleavage is central to the in vivo benefits of APC.

2. PAR-1 plays an important role in the development of diabetic nephropathy (DN) and PAR-1 might therefore be an attractive therapeutic target to pursue in DN.

3. Experimental TCDD-elicited steatohepatitis is associated with coagulation cascade activation and PAR-1-driven hepatic inflammation and fibrosis.

4. PAR1 in its inactive unligated state functions as a scaffold for TGFbetaRII to downregulate TGF-beta signaling, and thereby promote embryonic stem cell transition to functional endothelial cells.

5. this study shows that poly I:C treated PAR-1-/- mice given the thrombin inhibitor dabigatran etexilate exhibited less IFNbeta and CXCL10 expression in the spleen and plasma

6. Brain water content in the ipsilateral hemisphere and the tumor mass were significantly lower in PAR-1 KO than WT mice at day 12 after implantation of glioma cells.

7. The results of this study suggested that polarized microglia occur dynamically after ICH and that PAR-1 plays a role in the microglia activation and polarization.

8. In this study, we found upregulation of several hemostasis-related genes, including the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-deleted MLL-AF9 cells. Similar to the effect of Runx1/Cbfb deletion, PAR-1 overexpression induced CDKN1A/p21 expression and attenuated proliferation in MLL-AF9 cells

9. our findings define a detrimental role of thrombin-activated PAR-1 in wound healing in mice with spinal cord injuries.

10. thrombin/PAR-1 interaction regulated MCP-1, TF, MCSF and IL-6 production.

11. Thrombin upregulates LCN2 through protease-activated receptor-1 activation and causes brain damage.

12. Matrix metalloproteinases (MMP) are effectors of hippocampal neuroplasticity in the adult central nervous system and that the MMP-1/protease-activated receptor-1 axis may play a role in neurogenesis following physiological and/or pathological stimuli.

13. Data indicate an involvement of protease-activated receptor-1 in the neuroinflammation mediated by Eomes(+) CD4(+) T cells.

14. Bladder PAR activation elicits urothelial MIF release and urothelial MIF receptor signaling at least partly through CXCR4 to result in abdominal hypersensitivity without overt bladder inflammation

15. Data suggest that the pro-fibrotic effects of protease-activated receptor PAR-1 require the presence of protease-activated receptor PAR-2.

16. Thrombin-PAR1 signaling, via nitric oxide and EPCR, promotes hematopoietic stem cell (HSC) mobilization. aPC-EPCR-PAR1 signaling promotes HSC retention in bone marrow.

17. Colonic adenocarcinoma growth was reduced in PAR-1-deficient mice. Stromal cell-associated PAR-1 as one thrombin target important for tumor outgrowth.

18. Interference with the thrombin-PAR1 system does not reduce the adverse effects of blood on germinal cells of the immature mouse brain.

19. Protease activated receptor-1 deficiency diminishes bleomycin-induced skin fibrosis

20. impairs host defense during pneumococcal pneumonia

Pig (Porcine) Coagulation Factor II (thrombin) Receptor (F2R) Interaktionspartner

1. Thrombin stimulates swine smooth muscle cell differentiation from peripheral blood mononuclear cells via protease-activated receptor-1, RhoA, and myocardin.

2. Thrombin induces a sustained contraction in the normal pulmonary artery, by activating PAR(1) and thereby increasing the sensitivity of the myofilament to Ca(2+).

Cow (Bovine) Coagulation Factor II (thrombin) Receptor (F2R) Interaktionspartner

1. MMP-1 promotes VEGFR2 expression and proliferation of endothelial cells through stimulation of PAR-1 and activation of NF-kappaB

2. PAR1 and PAR2 regulate endothelial NO synthase phosphorylation and activity through G(12/13) and G(q), delineating the signaling pathways by which the proteases act on protease-activated receptors to modulate endothelial functions.