Article
Mutation of residues in the C3dg region of human complement component C3 corresponding to a proposed binding site for complement receptor type 2 (CR2, CD21) does not abolish binding of iC3b or C3dg to CR2.
Journal of immunology (Baltimore, Md. : 1950) - 1 Mar 1995
Diefenbach R J, Isenman D E
Abstract excerpt
Most evidence points toward there being a shared binding site in complement receptor type 2 (CR2, CD21) for the complement ligand C3dg and the EBV surface envelope glycoprotein gp350/220. Indeed, synthetic peptide studies have suggested that the CR2-binding sites in human C3dg and EBV gp350/220 s...
Topics
- Amino Acid Sequence
- Animals
- Binding Sites
- Cell Line
- Complement C3b
- Humans
- In Vitro Techniques
- Mice
- Molecular Sequence Data
- Mutagenesis, Site-Directed
- Mutation
- Peptide Fragments
- Peptides
- Protein Engineering
- Receptors, Complement 3d
- Recombinant Fusion Proteins
- Rosette Formation