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Complement factor I, also known as C3b/C4b inactivator, is a protein that in humans is encoded by the CFI gene. Complement factor I (factor I) is a protein of the complement system , first isolated in 1966 in guinea pig serum , [ 5 ] that regulates complement activation by cleaving cell-bound or fluid phase C3b and C4b. [ 6 ]
Atypical hemolytic uremic syndrome (aHUS), also known as complement-mediated hemolytic uremic syndrome (not to be confused with hemolytic–uremic syndrome), is an extremely rare, life-threatening, progressive disease that frequently has a genetic component. In most cases, it can be effectively controlled by interruption of the complement cascade.
CD46 complement regulatory protein also known as CD46 (cluster of differentiation 46) and Membrane Cofactor Protein is a protein which in humans is encoded by the CD46 gene. [5] CD46 is an inhibitory complement receptor .
First, the proteolytic component of the convertase, Bb, is removed by complement regulatory proteins having decay-accelerating factor (DAF) activity. Next, C3b is broken down progressively to first iC3b, then C3c + C3dg, and then finally C3d. Factor I is the protease cleaves C3b but requires a cofactor (e.g Factor H, CR1, MCP or C4BP) for activity.
Mothers who are negative for the Kell 1 antigen develop antibodies after being exposed to red blood cells that are positive for Kell 1.Over half of the cases of hemolytic disease of the newborn owing the anti-Kell antibodies are caused by multiple blood transfusions, with the remainder due to a previous pregnancy with a Kell 1 positive baby.
Complement receptor type 1 (CR1) also known as C3b/C4b receptor or CD35 (cluster of differentiation 35) is a protein that in humans is encoded by the CR1 gene. [ 3 ] [ 4 ] This gene is a member of the regulators of complement activation (RCA) family and is located in the 'cluster RCA' region of chromosome 1.
Factor I requires a C3b-binding protein cofactor such as complement factor H, CR1, or membrane cofactor of proteolysis (MCP or CD46) Complement factor H can inhibit the formation of the C3 convertase by competing with factor B for binding to C3b; [ 1 ] accelerate the decay of the C3 convertase; [ 2 ] and act as a cofactor for factor I-mediated ...
The cause of the condition lies in conception or utero with the aggregation of two distinct zygotes or blastocysts (one of which expresses 46,XX and the other of which expresses 46,XY) into a single embryo, [4] which subsequently leads to the development of a single individual with two distinct cell lines, instead of a pair of fraternal twins.