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Factor B KO Mouse on C57/Bl/6 Genetic Background

The Technology: Researchers at the University of Texas Health Science Center at Houston (UTHSC-H) have developed complement factor B-deficient mice on C57Black6 background via the disruption of the murine Bf, exon 3 through exon 7. It is becoming increasingly clear that factor B plays an important role in the regulation of the alternative complement pathway. The role of factor B in disease pathogenesis, however, is unclear. This well-characterized model lacks the complement factor B, making it an excellent model for studying the role of the alternative complement pathway in immune complex mediated diseases.


Publications:
• Watanabe H, Garnier G, Circolo A, Wetsel RA, Ruiz P, Holers VM, Boackle SA, Colten HR, Gilkeson GS. Modulation of renal disease in MRL/lpr mice genetically deficient in the alternative complement pathway factor B. J Immunol. 2000 Jan 15;164(2):786-94.
• Ishikawa N, Nonaka M, Wetsel RA, Colten HR. Murine complement C2 and factor B genomic and cDNA cloning reveals different mechanisms for multiple transcripts of C2 and B. J Biol Chem. 1990 Nov 5;265(31):19040-6.
• Matsumoto. M., W., A. Fukuda, J. Circolo, J. Goellner, X. Strauss-Schoenberger, S. Wang, T. Fujita, D. D. Hidvegi, D. D. Chaplin, H. R. Colten. 1997. Abrogation of the alternative complement pathway by targeted deletion of murine factor B. Proc. Natl. Acad. Sci. USA 94:8720.

UTHSC-H Ref. No.: 2007-0021 RMD
Inventors: Wetsel, et al.
Patent Status: N/A
License Available: worldwide; non-exclusive

Download Summary (2007-0021)