The serine protease, C1r, initiates activation of the classical pathway of complement, which
is a crucial innate defense mechanism against pathogens and altered-self cells. C1r both
autoactivates and subsequently cleaves and activates C1s. Because complement is
implicated in many inflammatory diseases, an understanding of the interaction between C1r
and its target substrates is required for the design of effective inhibitors of complement
activation. Examination of the active site specificity of C1r using phage library technology …