loading...| Preferred Name | GP1b-IX-V activation signalling | |
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| Definitions |
Authored: Akkerman, JW, 2009-06-03 Edited: Jupe, S, 2010-06-07 The platelet GPIb complex (GP1b-IX-V) together with GPVI are primarily responsible for regulating the initial adhesion of platelets to the damaged blood vessel and platelet activation. The importance of GPIb is demonstrated by the bleeding problems in patients with Bernard-Soulier syndrome where this receptor is either absent or defective. GP1b-IX-V binds von Willebrand Factor (vWF) to resting platelets, particularly under conditions of high shear stress. This transient interaction is the first stage of the vascular repair process. Activation of GP1b-IX-V on exposure of the fibrous matrix following atherosclerotic plaque rupture, or in occluded arteries, is a major contributory factor leading to thrombus formation leading to heart attack or stroke. GpIb also binds thrombin (Yamamoto et al. 1986), at a site distinct from the site of vWF binding, acting as a docking site for thrombin which then activates Proteinase Activated Receptors leading to enhanced platelet activation (Dormann et al. 2000). Reviewed: Kunapuli, SP, 2010-06-07 |
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| ID |
http://purl.obolibrary.org/obo/HINO_0015176 |
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| comment |
Authored: Akkerman, JW, 2009-06-03 Edited: Jupe, S, 2010-06-07 The platelet GPIb complex (GP1b-IX-V) together with GPVI are primarily responsible for regulating the initial adhesion of platelets to the damaged blood vessel and platelet activation. The importance of GPIb is demonstrated by the bleeding problems in patients with Bernard-Soulier syndrome where this receptor is either absent or defective. GP1b-IX-V binds von Willebrand Factor (vWF) to resting platelets, particularly under conditions of high shear stress. This transient interaction is the first stage of the vascular repair process. Activation of GP1b-IX-V on exposure of the fibrous matrix following atherosclerotic plaque rupture, or in occluded arteries, is a major contributory factor leading to thrombus formation leading to heart attack or stroke. GpIb also binds thrombin (Yamamoto et al. 1986), at a site distinct from the site of vWF binding, acting as a docking site for thrombin which then activates Proteinase Activated Receptors leading to enhanced platelet activation (Dormann et al. 2000). Reviewed: Kunapuli, SP, 2010-06-07 |
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| definition source |
Pubmed17597991 Pubmed2424116 Reactome, http://www.reactome.org Pubmed11001899 Pubmed15507277 Pubmed17585075 |
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| label |
GP1b-IX-V activation signalling |
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| prefixIRI |
HINO:0015176 |
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GP1b-IX-V activation signalling |
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| seeAlso |
ReactomeREACT_23847 Reactome Database ID Release 43430116 |
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http://purl.obolibrary.org/obo/HINO_0014395 http://purl.obolibrary.org/obo/HINO_0014399 http://purl.obolibrary.org/obo/HINO_0014397 http://purl.obolibrary.org/obo/HINO_0014382 http://purl.obolibrary.org/obo/HINO_0014410 |