Anti-CD59 antibody [EPR22394-242] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

CD59 also known as protectin is a protein with a molecular mass of approximately 18-25 kDa. It is widely expressed on the surface of many human cells including red blood cells and various types of leukocytes. CD59 serves as an inhibitor of the complement membrane attack complex (MAC) preventing cell lysis caused by terminal complement proteins. Through this mechanism it regulates complement activation and maintains cell integrity by halting the formation of MAC.

Biological function summary

One important feature of CD59 is its role as a glycosylphosphatidylinositol (GPI)-anchored protein involved in safeguarding cells from complement-mediated damage. It does not exist within a larger complex but functions at the cell surface to inhibit the assembly of complement components C5b-9 which form the MAC. This ability to inhibit MAC is essential in maintaining self-tissue from unintended damage during immune responses.

Pathways

CD59 participates in the regulation of the complement cascade specifically within the terminal pathway. The complement system serves as a bridge between innate and adaptive immunity contributing to processes like opsonization and cell lysis. CD59's inhibitory action directly impacts pathways that utilize terminal components such as C5b. Effective CD59 function prevents excessive complement activation ensuring that an immune response does not damage host tissues. It links closely with other complement regulatory proteins like CD55 which also mitigate complement cascade activation.

Associated diseases and disorders

Deficiencies or malfunctions in CD59 have notable implications. Paroxysmal nocturnal hemoglobinuria (PNH) is a disorder where lack of CD59 expression on blood cells leads to their increased destruction due to unregulated complement activity. Furthermore CD59's dysfunction or inadequacy also associates with atypical hemolytic uremic syndrome (aHUS) which involves mutant complement regulatory proteins causing overactivation of the complement system. These associations highlight the importance of CD59 in both maintaining cellular health and preventing pathophysiological conditions related to complement overactivity.