Biotin Anti-P-Selectin (CD62P) antibody [AK4]

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CD62P also known as P-selectin is a cell adhesion molecule expressed on the surface of activated endothelial cells and platelets. It is a type of protein with a known molecular weight of approximately 140 kDa. P-selectin plays a mechanical role in mediating leukocyte rolling on the endothelium which is an initial step in the inflammatory response. This protein is rapidly translocated to the plasma membrane upon platelet activation and is stored in alpha granules of platelets and Weibel-Palade bodies of endothelial cells.

Biological function summary

P-selectin is critical in the recruitment of leukocytes to sites of tissue injury and infection. It facilitates the adhesion of leukocytes to the vascular endothelium by binding to its ligand PSGL-1 on the leukocyte surface. This interaction supports the transition of leukocytes from the circulation to the site of inflammation. P-selectin is also involved in thrombus formation as it contributes to the interactions between platelets leukocytes and endothelium in the vascular wall. It acts as part of a dynamic complex in the regulation of the innate immune response and hemostasis.

Pathways

CD62P plays an important role in both the inflammatory and coagulation pathways. It is an important mediator in the leukocyte adhesion cascade influencing leukocyte tethering and rolling on activated endothelium. The interaction of P-selectin with PSGL-1 initiates the signaling pathways that lead to firm adhesion and extravasation of leukocytes. In the coagulation pathway P-selectin enhances interactions between platelets and leukocytes which support thrombus formation. Its regulation and activity are tightly linked with other proteins such as E-selectin and L-selectin in coordinating vascular and systemic inflammatory responses.

Altered expression of CD62P is associated with various inflammatory conditions and cardiovascular diseases. In thrombosis increased levels of P-selectin enhance platelet aggregation and stability of the thrombus contributing to pathological clot formation. Similarly in atherosclerosis P-selectin facilitates the recruitment of monocytes to the vessel wall promoting plaque development. The protein's function relates to interactions with key inflammatory mediators and its dysregulation is often observed in conditions like chronic inflammatory diseases and acute myocardial infarction.