|Calculated MW||This protein is fused with 6×His tag at the C-terminus, has a calculated MW of 35.8 kDa. The predicted N-terminus is Asp 35 . DTT-reduced Protein migrates as 50-65 kDa due to glycosylation.|
|Other Names||CD55, DAF, CR, CROM, TC|
|Results||Measured by its binding ability in a functional ELISA. When rhCD55 is coated at 1 µg/ml (100 µl/well), the concentration of rhCD97 that produces 50% of the optimal binding response is found to be approximately 0.15-2.0 µg/ml.|
|Application Notes||Centrifuge the vial prior to opening. Reconstitute in sterile PBS, pH 7.4 to a concentration of 50 µg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 month. For extended storage, it is recommended to store at -20°C.|
|Storage||-20°C; Lyophilized from 0.22 µm filtered solution in PBS, pH7.4. Normally Mannitol or Trehalose is added as protectants before lyophilization.|
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Provided below are standard protocols that you may find useful for product applications.
CD55, also known as DAF or decay accelerating factor, is a member of the RCA (regulators of complement activation) family characterized by four to 30 SCRs (short consensus repeats) in their plasma-exposed regions. CD55 /DAF is a 70 kDa membrane protein that regulates the complement system on the cell surface. It prevents the assembly of the C3bBb complex (the C3-convertase of the alternative pathway) or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex. This glycoprotein is broadly distributed among hematopoietic and non-hematopoietic cells. It is a determinant for the Cromer blood group system. CD55 is known to bind CD97 via the first SCR. It also binds physiologically generated C3 convertases with its second and third SCRs. Binding results in an accelerated “decay”, or dissociation of active C3 convertases, thus blocking the development of C’ attack complexes on non-foreign cells. Finally, viruses and bacteria are also known to utilize multiple SCR sites for infection.
Caras I.W.,et al.Nature 325:545-549(1987).
Osuka F.,et al.Genomics 88:316-322(2006).
Kalnine N.,et al.Submitted (MAY-2003) to the EMBL/GenBank/DDBJ databases.
Gregory S.G.,et al.Nature 441:315-321(2006).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.
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