Results 161 to 170 of about 6,222 (193)
Some of the next articles are maybe not open access.
Relative antithrombotic effect of soluble GPVI dimer compared with anti-GPVI antibodies in mice
Blood, 2005AbstractGlycoprotein VI (GPVI) is an essential platelet collagen receptor; therefore, the inhibition of GPVI-collagen interactions may be an attractive antithrombotic strategy. We have previously shown that targeting of GPVI with antibodies leads to the depletion of the receptor and to long-term antithrombotic protection in mice.
Sabine, Grüner +7 more
openaire +2 more sources
GPVI and integrin αIIbβ3 signaling in platelets [PDF]
Owen J T McCarty +2 more
exaly +2 more sources
The Journal of Pharmacology and Experimental Therapeutics, 2012
Glycoprotein VI (GPVI) has been proposed as a promising antiplatelet target, because its blockade prevents experimental thrombosis without impairing hemostasis. The objective of this study was to develop a preclinical tool to evaluate the role of human GPVI (hGPVI) in various models of thrombosis and to screen anti-GPVI compounds.
Mangin, Pierre +7 more
openaire +2 more sources
Glycoprotein VI (GPVI) has been proposed as a promising antiplatelet target, because its blockade prevents experimental thrombosis without impairing hemostasis. The objective of this study was to develop a preclinical tool to evaluate the role of human GPVI (hGPVI) in various models of thrombosis and to screen anti-GPVI compounds.
Mangin, Pierre +7 more
openaire +2 more sources
Blood, 2009
The search is on for natural regulators of platelet reactivity. In this issue of Blood, Trifiro and colleagues confirm that the low frequency isoform of platelet GPVI (VIb) attenuates ligand-mediated signal transduction and dampens down platelet reactivity with collagen while not affecting GPVI receptor copy number.
openaire +2 more sources
The search is on for natural regulators of platelet reactivity. In this issue of Blood, Trifiro and colleagues confirm that the low frequency isoform of platelet GPVI (VIb) attenuates ligand-mediated signal transduction and dampens down platelet reactivity with collagen while not affecting GPVI receptor copy number.
openaire +2 more sources
GPVI and the not so eager cleaver
Blood, 2010Platelets control their responsiveness, in part, by shedding adhesion and signaling receptors from their surface. The molecular mechanism by which this occurs, however,is incompletely understood. In this issue of Blood, Bender and colleagues make judicious use of mice genetically deficient in selected candidate proteases to shed new light on the ...
openaire +2 more sources
Highly potent anti-human GPVI monoclonal antibodies derived from GPVI knockout mouse immunization
Thrombosis Research, 2007Recent progress in the understanding of thrombus formation has suggested an important role for glycoprotein (GP) VI in this process. To clarify the exact role in detail, it is necessary to use specific, high affinity inhibitory antibodies. However, possibly due to the conserved structure of GPVI among species, it has been difficult to obtain potent ...
Yutaka, Matsumoto +9 more
openaire +2 more sources
Purification and characterisation of the platelet-activating GPVI/FcRγ complex in SMALPs [PDF]
The collagen/fibrin(ogen) receptor, glycoprotein VI (GPVI), is a platelet activating receptor and a promising anti-thrombotic drug target. However, while agonist-induced GPVI clustering on platelet membranes has been shown to be essential for its ...
Xueqing Wang
exaly +2 more sources
Generation of Transgenic Mice for Platelet-Specific Expression of Human GPVI From GPVI-Knockout Mice
Blood, 2011Abstract Abstract 1139 Transgenic mice with human gene knock-in (KI) in platelets can be very useful tools for the evaluation of anti-thrombotic therapeutics in vivo, as many murine thrombosis models have been established and well-characterized.
Bing Sun +5 more
openaire +1 more source
GPVI: no magic bullet for thrombosis
Blood, 2006Comment on Mangin et al, page The platelet collagen receptor GPVI has been considered an attractive therapeutic target to treat human cardiovascular diseases. An article by Mangin and colleagues in this issue of Blood reveals that loss of GPVI does not produce the expected dramatic effect on arterial thrombosis in mice.
openaire +1 more source

