Glycoprotein VI (Platelet) Proteins (GP6)

Human Glycoprotein VI (Platelet) (GP6) interaction partners

1. there is an altered activation state of GPVI signaling in ST-elevation myocardial infarction patients; GPVI is critical for the formation of arterial thrombosis in vivo

2. haplotype PEAN associated with SPS (show SMS Proteins) and manifested by fetal loss and suggest that the mechanism involved in the action of GPVI has significant effect on GPVI-mediated signal transduction through Syk (show SYK Proteins)-phosphorylation.

3. This suggests whereas platelet receptor shedding is mainly modulated by calcium-dependent signals, either platelet-surface interactions with the container walls during storage or induced shear stress under long-term agitation, might be also involved in the excessive shedding of GPVI during the storage of PRP (show C4BPA Proteins)-platelet concentrates.

4. There was no evidence to suggest that polymorphisms of GP VI T13254C and GP Ibalpha VNTR were associated with CAD.

5. Platelet adhesion to collagen induces GPVI dimer clustering. GPVI clustering increases both avidity for collagen and the proximity of GPVI-associated signaling molecules, which may be crucial for the initiation and persistence of signaling

6. Loss of the platelet surface receptors GPIbalpha (show GP1BA Proteins) and GPVI in heart failure, CF-VAD (show KCTD1 Proteins) and ECMO patients may contribute to ablated platelet adhesion/activation, and limit thrombus formation under high/pathologic shear conditions

7. Novel antithrombotic peptides derived from trowaglerix that acts through GPVI antagonism with greater safety-no severe bleeding.

8. results support the idea that genetic variability of GP6 regulatory regions can be associated with platelet hyperaggregability - a possible cause of miscarriage

9. These results demonstrate that GP6 is a receptor for fibrin and provide evidence that this interaction contributes to thrombus growth and stability.

10. data suggest a novel role for FAK (show PTK2 Proteins) in GPVI-dependent ROS (show ROS1 Proteins) formation and platelet activation and elucidate a proximal signaling role for FAK (show PTK2 Proteins) within the GPVI pathway.

Mouse (Murine) Glycoprotein VI (Platelet) (GP6) interaction partners

1. Platelet-specific deletion of GPVI does not lead to enhanced systemic inflammation and accelerated organ injury in two mouse models of sepsis

2. Tspan9 (show TSPAN9 Proteins) regulates platelet collagen receptor GPVI lateral diffusion and activation.

3. In conclusion, the present study unraveled ceramidase as a crucial player in sphingosine-induced platelet activation following GPVI-dependent signaling.

4. These results reveal a novel and unexpected function of hepatic Fc-gamma-RIIB in the targeted downregulation of GPVI in vivo.

5. collagen-I-mediated inhibition of proplatelet formation is specifically controlled by GPVI.

6. platelet GP6 and thromboxane A2 receptor (show TBXA2R Proteins) have a role in promoting inflammatory macrophage phenotype in skin inflammation

7. Novel antithrombotic peptides derived from trowaglerix that acts through GPVI antagonism with greater safety-no severe bleeding.

8. TULA-2 (show STS1 Proteins) Protein Phosphatase Suppresses Activation of Syk (show SYK Proteins) through the GPVI Platelet Receptor for Collagen by Dephosphorylating Tyr (show TYR Proteins)(P)346, a Regulatory Site of Syk (show SYK Proteins).

9. Inhibition of platelet activation by an anti-GPVI antibody significantly reduces infarct size.

10. These results demonstrate that GPVI is a receptor for fibrin and provide evidence that this interaction contributes to thrombus growth and stability.