Synthetic peptide directed towards the C terminal region of human GP1BA
Application
Anti-GP1BA antibody produced in rabbit is suitable for western blotting at a concentration of 0.25μg/ml.
Biochem/physiol Actions
Glycoprotein Ib (GP1BA) is a membrane glycoprotein present on the surface of platelets. It acts as the receptors for von Willebrand factor that facilitates the adhesion of platelets to vascular subendothelium after vascular injury, thrombosis, platelet activation and hemostasis. Mutations in GP1BA are associated with Bernard-Soulier syndromes and platelet-type von Willebrand disease.
Sequence
Synthetic peptide located within the following region: RGSLPTFRSSLFLWVRPNGRVGPLVAGRRPSALSQGRGQDLLSTVSIRYS
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Seminars in thrombosis and hemostasis, 39(6), 663-673 (2013-08-13)
Compared with coagulation factor defects, little attention is given to defects of platelet function as causes of rare bleeding disorders. Platelet-type von Willebrand disease (PT-VWD) is an autosomal dominant bleeding disorder and is unique among platelet disorders because it is
A defective platelet glycoprotein (GP) Ib/IX/V complex [von Willebrand factor (VWF) receptor] results in Bernard-Soulier syndrome (BSS), which is characterized by macrothrombocytopenia and impaired ristocetin- and thrombin-induced platelet aggregation. We found 2 independent BSS-variant families: Case I [compound heterozygous mutations
Aspirin is an antiplatelet agent commonly used in treatment of patients with high risk to develop stroke and myocardial infarction. However, inter-individual variability regarding the inhibition of platelet function by aspirin is well documented. In this study, the correlation between
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