The protein which is capable of controlling the clotting of blood by preventing blood platelets sticking together has been discovered by a research team belonging to the University of North Carolina. Several deaths are caused by interactions between blood platelets when strokes and heart attacks take place, which are altogether uncontrolled.
The GPIIb/IIIa is kept in an inactive state by the CIB1. The interactions between platelets in the blood are also prevented because of this. The CIB1 thus plays the role of a gatekeeper with regard to GPIIb/IIIa activation. The CIB1 protein was discovered in 1997 inside platelets which binds to GPIIb/IIIa.
The GPIIb/IIIa which is normally inactive becomes activated during the course of clotting. New therapeutic approaches may result from the knowledge with regard to the functions of the CIB1. The GPIIb/IIIa was seen to become more responsive with the decrease of CIB1 in the cells, while GPIIb/IIIa activation is prevented with the higher amounts of CIB1.
A platelet remains inactive so long as the GPIIb/IIIa and the CIB1 are bound together. While the adhesion receptor is bound to the CIB1, the talin is prevented from activating and binding the receptor. Further studies are planned with regard to the mechanisms of interaction between the CIB1/GPIIb/IIIa, which will lead to better therapies being developed.