Factor B KO Mouse on C57/Bl/6 Genetic Background
The Technology: Researchers at the University of Texas
Health Science Center at Houston (UTHealth) 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.
UTHealth Ref. No.: 2007-0021
Inventors: Wetsel, et al.
License Available:
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