The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

Cfb  -  complement factor B

Mus musculus

Synonyms: AI195813, AI255840, Bf, C2, C3/C5 convertase, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Cfb

  • OBJECTIVE: To investigate the effect of complement deficiency on atherogenesis and lipidemia, we used mice deficient in the third complement component (C3-/-) or factor B (FB-/-) [1].
  • Factor B represented approximately 0.5% of newly synthesized protein and 4-6% of the secreted protein of resident peritoneal macrophages and macrophages elicited with thioglycollate broth, pyran copolymer, NaIO4, bacillus Calmette-Guerin, or Corynebacterium parvum [2].
  • Two factor B messenger RNA transcripts are expressed in kidney and intestine; SLE nephritis is associated with decrease in the long factor B mRNA and increase in the short form [3].
  • Sensitivity to lethal endotoxic shock was not significantly altered in Bf-deficient mice [4].
  • To ascertain the functional consequences of this polymorphism in the Bf promoter, we analyzed the effects of strain-specific sequences in the Bf 5' region on the expression of a chloramphenicol acetyltransferase (CAT) reporter gene transfected in human and mouse hepatoma cells [5].
 

High impact information on Cfb

  • Introducing a second mutation in the gene encoding complement factor B, which prevents C3 turnover in vivo, obviates the phenotype of Cfh(-/-) mice [6].
  • Properdin, the terminal complement components, thrombospondin and the circumsporozoite protein of malaria parasites contain similar sequence motifs [7].
  • Properdin is a plasma glycoprotein which stabilizes the C3bnBb enzyme complex of the alternative pathway of the complement system [7].
  • Biosynthesis of membrane factor B by mouse peritoneal macrophages [8].
  • In particular, there is evidence for the membrane-associated factor B in human lymphocytes [8].
 

Chemical compound and disease context of Cfb

  • These results suggest that: 1) factor B plays an important role in the pathogenesis of glomerulonephritis and vasculitis in MRL/lpr mice; and 2) activation of the alternative pathway, either by the amplification loop or by IgA immune complexes, has a prominent effect on serum C3 levels in this lupus model [9].
  • Notably, thrombus formation was absent in spleens of C2/factor B(-/-) mice, suggesting that the alternative complement pathway contributes to shock-induced intravascular coagulation [10].
  • In the NZB/W F1 hybrid strain, coincident with the development of glomerulonephritis a marked increase in kidney C3 and C4 mRNA was observed; Factor B mRNA, which is expressed as a doublet in kidney and intestine, showed an increase in expression of the smaller transcript [11].
  • With these results, we combined perifosine and temozolomide as treatment of platelet-derived growth factor B-driven gliomas in mice [12].
  • Nevertheless, abolition of tumor-induced antiinflammation follows injection of tumorous ascites by a mechanism that involves Factor B suppression of the corticosterone response to the tumor while Factor A apparently raises the threshold at which physiological increases in corticosterone inhibit leukocyte emigration [13].
 

Biological context of Cfb

  • Studies in factor B-deficient mice, however, indicate that alternative pathway activation is required and amplifies complement activation [14].
  • MRL/lpr Bf-/- mice developed less renal disease and had improved survival; however, these mice were also a different major histocompatibility complex (MHC) haplotype (H-2b) than their wild-type littermates (H-2k) due to the gene for Bf being located in the MHC gene complex [15].
  • The Bf mRNA remained undetectable, whereas a readily detectable C3 mRNA level reappeared, in diestrus [16].
  • Ovarian steroid-regulated synthesis and secretion of complement C3 and factor B in mouse endometrium during the natural estrous cycle and pregnancy period [16].
  • The genetic linkage between S locus and Bf locus was studied with two backcross progenies--[B10.BR X (B10.BR X Mus m. subspecies Chc)F1] and [B10.BR X (B10.BR X Mus m. subspecies Shh)F1] [17].
 

Anatomical context of Cfb

 

Associations of Cfb with chemical compounds

 

Physical interactions of Cfb

  • The results indicated that murine Bf was controlled by a single codominant locus located close to the H-2 complex because no mouse showing recombination between Bf locus and S locus was found [17].
  • Initiation of the alternative pathway is inhibited by CI already at the stage of cleavage of factor B. CI binds to C4, C4b, C3 and C3b; since the major inhibitory action of CI is lost after washing of cell intermediates, complex formation and, as a consequence, steric hindrance may be responsible for the inhibiting effects of CI [21].
  • Inhibition of the alternative pathway by factor B siRNA resulted in decreased levels of membrane attack complex and angiogenic factors-vascular endothelial growth factor and TGF-beta2 [22].
 

Regulatory relationships of Cfb

  • Northern analysis revealed that Bf mRNA expression was synergistically up-regulated by TNF-alpha and IFN-gamma in MH-S cells [23].
  • Macrophage factor B was cleaved and activated to factor Bb- and Ba-like fragments by factor D and cobra venom factor [2].
  • Constitutive expression of murine complement factor B gene is regulated by the interaction of its upstream promoter with hepatocyte nuclear factor 4 [5].
  • The absence of platelet-derived growth factor-B in circulating cells promotes immune and inflammatory responses in atherosclerosis-prone ApoE-/- mice [24].
  • Regulation of C4 synthesis in the mouse macrophage is accomplished by mechanisms that are independent of this feedback control but the murine cells also display separate mechanisms for regulation of C4 and factor B-specific mRNA levels [25].
 

Other interactions of Cfb

  • IgG was detected in the glomeruli of diseased C1qa/H2-Bf/C2-/- kidneys [26].
  • Totally, 256 backcross progenies were typed for Bf type and for Ss type (plasma level of the fourth complement protein regulated by S locus) [17].
  • Structural polymorphism of murine factor B controlled by a locus closely linked to the H-2 complex and demonstration of multiple alleles [17].
  • On differentiation, mRNA for C3 (fivefold) and factor D (> 50-fold) increased, whereas stimulation with tumour necrosis factor (TNF)-alpha and interleukin (IL) 1 beta led to eightfold increases in factor B mRNA [20].
  • A previous study from our laboratory evaluated the development of renal disease in MRL/lpr mice genetically deficient in factor B (Bf-/-), a protein necessary for AP activation [15].
 

Analytical, diagnostic and therapeutic context of Cfb

References

  1. Lack of complement factor C3, but not factor B, increases hyperlipidemia and atherosclerosis in apolipoprotein E-/- low-density lipoprotein receptor-/- mice. Persson, L., Borén, J., Robertson, A.K., Wallenius, V., Hansson, G.K., Pekna, M. Arterioscler. Thromb. Vasc. Biol. (2004) [Pubmed]
  2. Factor B, the complement alternative pathway serine proteinase, is a major constitutive protein synthesized and secreted by resident and elicited mouse macrophages. Sundsmo, J.S., Chin, J.R., Papin, R.A., Fair, D.S., Werb, Z. J. Exp. Med. (1985) [Pubmed]
  3. Local extrahepatic expression of complement genes C3, factor B, C2, and C4 is increased in murine lupus nephritis. Passwell, J., Schreiner, G.F., Nonaka, M., Beuscher, H.U., Colten, H.R. J. Clin. Invest. (1988) [Pubmed]
  4. Abrogation of the alternative complement pathway by targeted deletion of murine factor B. Matsumoto, M., Fukuda, W., Circolo, A., Goellner, J., Strauss-Schoenberger, J., Wang, X., Fujita, S., Hidvegi, T., Chaplin, D.D., Colten, H.R. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  5. Constitutive expression of murine complement factor B gene is regulated by the interaction of its upstream promoter with hepatocyte nuclear factor 4. Garnier, G., Circolo, A., Colten, H.R. J. Biol. Chem. (1996) [Pubmed]
  6. Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H. Pickering, M.C., Cook, H.T., Warren, J., Bygrave, A.E., Moss, J., Walport, M.J., Botto, M. Nat. Genet. (2002) [Pubmed]
  7. Properdin, the terminal complement components, thrombospondin and the circumsporozoite protein of malaria parasites contain similar sequence motifs. Goundis, D., Reid, K.B. Nature (1988) [Pubmed]
  8. Biosynthesis of membrane factor B by mouse peritoneal macrophages. Ooi, Y.M., Ooi, B.S. Nature (1982) [Pubmed]
  9. Modulation of renal disease in MRL/lpr mice genetically deficient in the alternative complement pathway factor B. Watanabe, H., Garnier, G., Circolo, A., Wetsel, R.A., Ruiz, P., Holers, V.M., Boackle, S.A., Colten, H.R., Gilkeson, G.S. J. Immunol. (2000) [Pubmed]
  10. Central role of complement in passive protection by human IgG1 and IgG2 anti-pneumococcal antibodies in mice. Saeland, E., Vidarsson, G., Leusen, J.H., Van Garderen, E., Nahm, M.H., Vile-Weekhout, H., Walraven, V., Stemerding, A.M., Verbeek, J.S., Rijkers, G.T., Kuis, W., Sanders, E.A., Van De Winkel, J.G. J. Immunol. (2003) [Pubmed]
  11. Complement gene expression in hepatic and extrahepatic tissues of NZB and NZB x W (F1) mouse strains. Passwell, J.H., Schreiner, G.F., Wetsel, R.A., Colten, H.R. Immunology (1990) [Pubmed]
  12. Perifosine inhibits multiple signaling pathways in glial progenitors and cooperates with temozolomide to arrest cell proliferation in gliomas in vivo. Momota, H., Nerio, E., Holland, E.C. Cancer Res. (2005) [Pubmed]
  13. On the mechanism of antiinflammation induced by tumor transplantation, surgery, and irritant injection. Normann, S., Besedovsky, H., Schardt, M., del Rey, A. J. Leukoc. Biol. (1991) [Pubmed]
  14. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. Girardi, G., Berman, J., Redecha, P., Spruce, L., Thurman, J.M., Kraus, D., Hollmann, T.J., Casali, P., Caroll, M.C., Wetsel, R.A., Lambris, J.D., Holers, V.M., Salmon, J.E. J. Clin. Invest. (2003) [Pubmed]
  15. Effects of complement factor D deficiency on the renal disease of MRL/lpr mice. Elliott, M.K., Jarmi, T., Ruiz, P., Xu, Y., Holers, V.M., Gilkeson, G.S. Kidney Int. (2004) [Pubmed]
  16. Ovarian steroid-regulated synthesis and secretion of complement C3 and factor B in mouse endometrium during the natural estrous cycle and pregnancy period. Li, S.H., Huang, H.L., Chen, Y.H. Biol. Reprod. (2002) [Pubmed]
  17. Structural polymorphism of murine factor B controlled by a locus closely linked to the H-2 complex and demonstration of multiple alleles. Natsuume-Sakai, S., Moriwaki, K., Migita, S., Sudo, K., Suzuki, K., Lu, D.Y., Wang, C., Takahashi, M. Immunogenetics (1983) [Pubmed]
  18. A targeted disruption of the murine complement factor B gene resulting in loss of expression of three genes in close proximity, factor B, C2, and D17H6S45. Taylor, P.R., Nash, J.T., Theodoridis, E., Bygrave, A.E., Walport, M.J., Botto, M. J. Biol. Chem. (1998) [Pubmed]
  19. Regulation of alternative pathway activation and C3a production by adipose cells. Choy, L.N., Spiegelman, B.M. Obes. Res. (1996) [Pubmed]
  20. Detection and quantification of the control proteins of the alternative pathway of complement in 3T3-L1 adipocytes. Peake, P.W., O'Grady, S., Pussell, B.A., Charlesworth, J.A. Eur. J. Clin. Invest. (1997) [Pubmed]
  21. Isolation and properties of a complement inhibitor from Naja haje venom, distinct from known anticomplementary factors in cobra venom. von Zabern, I., Przyklenk, H., Damerau, B., Zimmermann, B. Scand. J. Immunol. (1981) [Pubmed]
  22. Complement activation via alternative pathway is critical in the development of laser-induced choroidal neovascularization: role of factor B and factor H. Bora, N.S., Kaliappan, S., Jha, P., Xu, Q., Sohn, J.H., Dhaulakhandi, D.B., Kaplan, H.J., Bora, P.S. J. Immunol. (2006) [Pubmed]
  23. Complement factor B gene regulation: synergistic effects of TNF-alpha and IFN-gamma in macrophages. Huang, Y., Krein, P.M., Muruve, D.A., Winston, B.W. J. Immunol. (2002) [Pubmed]
  24. The absence of platelet-derived growth factor-B in circulating cells promotes immune and inflammatory responses in atherosclerosis-prone ApoE-/- mice. Tang, J., Kozaki, K., Farr, A.G., Martin, P.J., Lindahl, P., Betsholtz, C., Raines, E.W. Am. J. Pathol. (2005) [Pubmed]
  25. Expression of the MHC class III genes. Colten, H.R. Philos. Trans. R. Soc. Lond., B, Biol. Sci. (1984) [Pubmed]
  26. Cutting edge: C1q protects against the development of glomerulonephritis independently of C3 activation. Mitchell, D.A., Taylor, P.R., Cook, H.T., Moss, J., Bygrave, A.E., Walport, M.J., Botto, M. J. Immunol. (1999) [Pubmed]
  27. Tissue-specific initiation of murine complement factor B mRNA transcription. Nonaka, M., Ishikawa, N., Passwell, J., Natsuume-Sakai, S., Colten, H.R. J. Immunol. (1989) [Pubmed]
 
WikiGenes - Universities