Description
Product Characteristics: The monoclonal antibody 3D5 recognizes complement decay accelerating factor (DAF), also designated as CD55. Cells express on their surface several proteins which protect against complement attack, namely C receptor I (CR1), decay accelerating factor (DAF), membrane cofactor protein (MCP) and CD59. CR1, DAF and MCP regulate the activation pathways of complement by either accelerating decay of the C3 and C5 convertase (CR1, DAF), or acting as cofactors for the serine protease factor I, which cleaves and irreversibly inactivates C3b (CR1, MCP). Mouse DAF (CD55) is a 60 kDa transmembrane protein that binds C3b and C4b to inhibit formation and half-life of the C3 convertases. DAF is broadly distributed among cells in contact with serum, including both haematopoietic and nonhaematopoietic cells. Although DAF does not have an essential role in controlling hemolysis of erythrocytes, it has an important role in regulation of the deposition of C3 on nucleated cells. Together with other complement regulators DAF protects self cells from autologous complement- mediated injury. DAF cooperates with CD46 in circumventing autologous C3 deposition, while CD59 inhibits the pathway at the critical end-point. Aliases DAF (decay accelerating factor), CD55 Immunogen NRK cells expressing transmembrane-anchored mouse DAF
Target Information: This gene encodes a protein involved in the regulation of the complement cascade. The encoded glycoprotein is also known as the decay-accelerating factor (DAF)\, binding of DAF to complement proteins accelerates their decay, disrupting the cascade and preventing damage to host cells. Antigens present on the DAF glycoprotein constitute the Cromer blood group system (CROM). Two alternatively spliced transcripts encoding different proteins have been identified. The predominant transcript encodes a membrane-bound protein expressed on cells exposed to plasma component proteins but an alternatively spliced transcript produces a soluble protein present at much lower levels. Additional, alternatively spliced transcript variants have been described, but their biological validity has not been determined. [provided by RefSeq, Jul 2008]