Decay accelerating factor is a 70 kDa membrane protein that regulates the complement system on the cell surface.

Immunocytochemistry techniques have found decay accelerating factor (DAF) protein on the tegument.

C3-convertase can be inhibited by Decay accelerating factor (DAF), which is bound to erythrocyte plasma membranes via a GPI anchor.

Pigs lacking alpha-Gal or overexpressing human Decay Accelerating Factor (hDAF), amongst others, have been generated to study the impact on transplanted outcome in nonhuman primate models.

The Dr adhesins bind Dr blood group antigen (Dr) which is present on decay accelerating factor (DAF) on erythrocytes and other cell types.

This protein does not interact with the complement regulatory protein, decay accelerating factor CD55, unlike the related CD97 antigen, and indicates that these very closely related proteins likely have nonredundant functions.

These mediate binding to its cellular ligand, decay accelerating factor (DAF/CD55), a regulatory protein of the complement cascade, however the CD55-CD97 interaction is believed to have an activity independent of complement.

Decay-accelerating factor (DAF) is another negative regulator of C3 convertase.

Decay-accelerating factor (DAF or CD55)

First, the proteolytic component of the convertase, Bb, is removed by complement regulatory proteins having decay-accelerating factor (DAF) activity.

Mutations affecting GPI that reduce expression of CD59 and decay-accelerating factor on red blood cells result in paroxysmal nocturnal hemoglobinuria.

Complement decay-accelerating factor, also known as CD55 or DAF, is a protein that, in humans, is encoded by the CD55 gene.

The Dr family of adhesins bind to the Dr blood group antigen component of decay-accelerating factor (DAF).

Echoviruses and coxsackie B viruses that use human decay-accelerating factor (DAF) as a receptor do not bind the rodent analogues of DAF.

The hyperacute rejection reaction is known to be mediated by complement which in itself is regulated by a family of membrane glycoproteins including decay-accelerating factor (DAF) and membrane cofactor protein.

In PNH a clonal defect in blood stem cells in the gene PIGA, that is required for GPI synthesis, results in faulty GPI linkage of decay-accelerating factor (DAF) and CD59 in red blood cells.