Cfb Conditional Knockout mouse models

Cfb is the mouse ortholog of human CFB and encodes complement factor B, the catalytic engine of the alternative pathway. The zymogen comprises three complement control protein modules, a von Willebrand factor type A domain that coordinates magnesium, and a chymotrypsin-like serine protease domain; binding to surface-bound C3b or hydrolyzed C3 opens the molecule for factor D cleavage into Ba and Bb, leaving Bb as the proteolytic subunit of the C3bBb convertase that properdin stabilizes and factor H and decay accelerating factor dissociate. Gain-of-function variants such as human D279G and F286L create decay-resistant convertases and cause atypical hemolytic uremic syndrome and C3 glomerulopathy. Nulls are viable with an intact classical pathway, cleanly isolating amplification loop contributions. Introduce patient missense knockins when spontaneous complement-driven renal disease is the goal, hepatocyte-conditional deletion when the source of circulating factor B matters, and humanization when iptacopan class inhibitors are being profiled.

A floxed Cfb allele paired with Cre gives spatial control that whole body knockouts cannot offer. People use it to separate developmental roles from adult homeostasis, to model somatic mutations, and to match disease that begins in one organ.