CD42b (GPIb alpha)
● Interaction with collagen-captured VWF to form the initial barrier to blood loss
● Propagate the clot via platelet aggregation
● Provide the platform for secondary haemostasis
● Localisation mechanisms
● Maintain endothelial junction integrity
Exposure of sub-endothelial collagen after vessel trauma promotes binding of VWF which tethers platelets via their GpIb receptor. Blood flow rolls the platelet over where it forms stable associations via separate collagen binding receptors which also serves to activate the platelet. Activated platelets change their shape to promote effective physical interaction and release of the contents of cytoplasmic granules which activate more platelets and promote platelet-to-platelet aggregation via fibrinogen bridging of receptors on adjacent platelets. Biochemical pathways are also activated to promote aggregation, and the phospholipid membrane re-organises to promote localisation of secondary haemostasis to stabilise the platelet plug.
Reduced platelet numbers, receptor deficiency/dysfunction, granule deficiency or granule content deficiency, biochemical abnormalilties and drug interactions can lead to bleeding disorders. Quantitative receptor deficiencies can be detected using labelled antibodies in flow cytometry.
The sample should be analysed within 4 hours of venepuncture and cannot be stored.
North Wing - 4th and 5th Floors
Westminster Bridge Road
London SE1 7EH
Laboratory opening times
Last updated: 07/08/2015