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Gene Review

CFI  -  complement factor I

Homo sapiens

Synonyms: AHUS3, ARMD13, C3B/C4B inactivator, C3BINA, C3b-INA, ...
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Disease relevance of CFI


Psychiatry related information on CFI

  • Expressed emotion (EE) in key relatives of 21 patients with bipolar affective or schizoaffective psychoses was assessed by the CFI [5].
  • The second phase consists in an illustration of the objectives and purpose of the Service. During this phase, two weekly interviews lasting approximately one hour are proposed, plus assessment tests (CFI, Camberwell Family Interview--and MMPI--Minnesota Multiphasic Personality Inventory) [6].
  • Supervisors completed the Countertransference Factors Inventory (CFI) with regard to their supervisees [7].
  • Forty-two children (ages 7-14) completed the Fantasy Questionnaire (FQ), the Children's Social Desirability Questionnaire (CSDQ), the Zelter and LeBaron (1984) revision of the Stanford Hypnotic Clinical Scale for Children (SHCS:C-R), and the Children's Fantasy Inventory: Absorption and Vividness Scales (CFI: A & V) [8].
  • Each participant completed one affective health-related questionnaire (Leeds Scales for the Self-Assessment of Anxiety and Depression; Snaith, Bridge & Hamilton, 1976) and their EE was rated using the Camberwell Family Interview (CFI; Brown, Birley & Wing, 1972; Vaughn & Leff, 1976, modified for head-injury relatives [9].

High impact information on CFI

  • Deletion of C3bINA and beta 1H from the complete mixture caused total consumption of C3 in the fluid phase and resulted in neither C3 binding to the complexes nor solubilization [10].
  • Immune precipitates were solubilized by the alternative pathway of complement assembled from isolated proteins, i.e., C3, factor B, factor D, properdin, C3b inactivator (C3bINA), and beta 1H [10].
  • Short-term cultures of human peripheral blood monocytes were shown to synthesize the alternative pathway complement components C3, factors B (B) and D (D), and properdin, the regulatory proteins C3b inactivator (C3bINA) and beta 1H, in addition to C2, C4, and C5 [11].
  • The increased numbers of C3b sites susceptible to inactivation by C3bINA in the presence of beta 1H were significantly correlated to the number of molecules of heparin/particle [12].
  • Native C4 was not affected by C3bINA aand C4-bp [13].

Chemical compound and disease context of CFI

  • 4. By univariate analysis, the following were predictors of CFI > or =0.25: high levels of high-density lipoprotein cholesterol, the absence of previous non-Q-wave myocardial infarction, angina pectoris during an exercise test, angiographic indicators of severe CAD and the left circumflex or right coronary artery as the collateral-receiving vessel [14].
  • The economical outpatient antibiotics of choice for CFI are penicillin plus dicloxacillin; the former is needed to cover Eikenella corrodens and the latter to cover Staphylococcus aureus, both common in these wounds [15].
  • In patients with Crohn's disease (CD) we investigated the C3 conversion of zymosan-activated serum (ZAS) and looked for the occurrence of chemotactic factor inactivation (CFI) [16].
  • There was an inverse relationship between CFI and DMFT in subjects aged 12-18 and a direct relationship between dental fluorosis and the fluoride content of well-water used for cooking and drinking [17].
  • Three of four animals inoculated with the LAV or HTLV-IIIB strain of HIV developed antibodies inhibiting CD4-dependent cell fusion by HIV glycoprotein (CFI-antibodies) 2-3 months after inoculation coincident with development of HIV specific IgG antibodies [18].

Biological context of CFI


Anatomical context of CFI

  • Insulin Growth Factor-I and Epidermal Growth Factor Receptors Recruit Distinct Upstream Signaling Molecules to Enhance AKT Activation in Mammary Epithelial Cells [24].
  • Of note are experiments by others and us who could not identify FI-specific mRNA in peripheral blood-derived monocytes, granulocytes, or B- and T-cells of man or rat and in rat peritoneal macrophages [1].
  • These data support the notion that FI in contrast to FH is not expressed by cells of the monocyte-macrophage lineage or by other leukocytes of peripheral blood, at least in the absence of additional stimulants [1].
  • Chemotactic factor inactivator (CFI) can decrease the neutrophil chemotactic activity of C5a [22].
  • The roles of complement levels and CFI activity in the regulation of chemotactic factor generation were evaluated in newborn and adult plasmas [25].

Associations of CFI with chemical compounds

  • FI, a highly glycosylated serine protease of 88 kDa cleaves the alpha-chains of both complement components C3b and C4b, thereby inactivating them [1].
  • The highly chemotactic synthetic peptide Met-Leu-Phe was completely hydrolyzed by CFI preparations [20].
  • CFI preparations readily hydrolyzed the peptide Arg-Phe-Ala [20].
  • The former has a specificity for inactivation of the chemotactic activity associated with the C3 fragments, whereas the C5 chemotactic fragment is specifically inactivated by the alpha-globulin CFI [26].
  • Trypsin-produced C5 leukotactic peptides can be converted into tumor cell chemotactic factors by treatment with tumor cell extracts or by incubation with the alpha-globulin chemotactic factor inactivator (CFI) isolated from human serum [27].

Regulatory relationships of CFI

  • The IL-6 induced increase in CFI gene expression was inhibited by actinomycin D indicating regulatory effects at the level of transcription [28].
  • The results showed that alternative pathway turnover was dependent upon C3 turnover, but failed to support the notion that levels of C3bINA or beta 1H control alternative pathway turnover in RA [29].

Other interactions of CFI

  • At lower concentrations the effect of EACA on C3bINA is apparently less significant; therefore, at low concentrations of EACA, its inhibitory effects on C3 cleavage by the properdin system in serum prediominate [30].
  • The enhancing effect of high concentrations of EACA on C3 cleavage in serum may be explained by its observed inhibition of C3b inactivator (C3bINA) [30].
  • Mutations in genes encoding other complement regulatory proteins, membrane cofactor protein (CD46) and complement factor I (CFI), were also involved in the pathogenesis of the disease [31].
  • There was a direct correlation between CFI and distal VEGF (r = 0.33, P = 0.05) but not bFGF concentrations [32].
  • Our results indicate that the upregulation of CFI gene expression by IL-6 involves a coordinate effort at the level of transcription and mRNA stability, with the enhanced rate of transcription being the principal mechanism [28].

Analytical, diagnostic and therapeutic context of CFI

  • Furthermore, the direct interaction of CFI with C5a and C5a des Arg was assessed by ELISA tests and column chromatography and no interaction was observed [22].
  • We suggest that the maintenance of or increase in CFI activity in patients undergoing hemodialysis enhances the clearance of circulating chemotactins, preventing the persistent activation of neutrophils during the procedure and subsequent organ dysfunction [33].
  • The chemotactic factor inactivator (CFI) has been isolated from whole human serum by a combination of techniques including salt precipitation, anionic exchange, and gel filtration chromatography [26].
  • Percent diameter stenosis of the lesion undergoing PTCA was the only independent predictor of a high CFI [14].
  • Sequence analysis revealed a close relationship between CFI and pyruvate carboxylase [34].


  1. Expression and regulation of complement factors H and I in rat and human cells: some critical notes. Schlaf, G., Demberg, T., Beisel, N., Schieferdecker, H.L., Götze, O. Mol. Immunol. (2001) [Pubmed]
  2. A mutation in factor I that is associated with atypical hemolytic uremic syndrome does not affect the function of factor I in complement regulation. Nilsson, S.C., Karpman, D., Vaziri-Sani, F., Kristoffersson, A.C., Salomon, R., Provot, F., Fremeaux-Bacchi, V., Trouw, L.A., Blom, A.M. Mol. Immunol. (2007) [Pubmed]
  3. Suppression of immune complex-induced inflammation by the chemotactic factor inactivator. Johnson, K.J., Anderson, T.P., Ward, P.A. J. Clin. Invest. (1977) [Pubmed]
  4. A chemotactic inhibitor produced by blast cells and present in the serum of a patient with acute lymphoblastic leukemia. Blumenfeld, W., Territo, M. Blood (1979) [Pubmed]
  5. Lithium prophylaxis and expressed emotion. Priebe, S., Wildgrube, C., Müller-Oerlinghausen, B. The British journal of psychiatry : the journal of mental science. (1989) [Pubmed]
  6. The organization of a counselling service for the families of patients undergoing bone marrow transplant. Invernizzi, G., Broich, G., Bressi, C., Guggeri, G., Caparrelli, S., Deliliers, G.L. Anticancer Res. (1999) [Pubmed]
  7. Countertransference management and therapy outcome: an initial evaluation. Gelso, C.J., Latts, M.G., Gomez, M.J., Fassinger, R.E. Journal of clinical psychology. (2002) [Pubmed]
  8. Correlates of hypnotizability in children: absorption, vividness of imagery, fantasy play, and social desirability. Plotnick, A.B., Payne, P.A., O'Grady, D.J. The American journal of clinical hypnosis. (1991) [Pubmed]
  9. A retrospective analysis of expressed emotion (EE) and affective distress in a sample of relatives caring for traumatically brain-injured (TBI) family members. Flanagan, D.A. The British journal of clinical psychology / the British Psychological Society. (1998) [Pubmed]
  10. Solubilization of immune precipitates by six isolated alternative pathway proteins. Fujita, T., Takata, Y., Tamura, N. J. Exp. Med. (1981) [Pubmed]
  11. Biosynthesis of the complement components and the regulatory proteins of the alternative complement pathway by human peripheral blood monocytes. Whaley, K. J. Exp. Med. (1980) [Pubmed]
  12. Surface-associated heparin inhibits zymosan-induced activation of the human alternative complement pathway by augmenting the regulatory action of the control proteins on particle-bound C3b. Kazatchkine, M.D., Fearon, D.T., Silbert, J.E., Austen, K.F. J. Exp. Med. (1979) [Pubmed]
  13. Human C4-binding protein. II. Role in proteolysis of C4b by C3b-inactivator. Fujita, T., Gigli, I., Nussenzweig, V. J. Exp. Med. (1978) [Pubmed]
  14. Frequency distribution of collateral flow and factors influencing collateral channel development. Functional collateral channel measurement in 450 patients with coronary artery disease. Pohl, T., Seiler, C., Billinger, M., Herren, E., Wustmann, K., Mehta, H., Windecker, S., Eberli, F.R., Meier, B. J. Am. Coll. Cardiol. (2001) [Pubmed]
  15. Controversies in antibiotic choices for bite wounds. Callaham, M. Annals of emergency medicine. (1988) [Pubmed]
  16. Humoral inhibition of neutrophil chemotaxis in Crohn's disease. D'Amelio, R., Pallone, F., Le Moli, S., Pontesilli, O., Ricci, R., Montano, S., Rossi, P. Scand. J. Immunol. (1985) [Pubmed]
  17. Dental caries experience in the Chiangmai/Lamphun provinces of Thailand. Songpaisan, Y., Davies, G.N. Community dentistry and oral epidemiology. (1989) [Pubmed]
  18. Induction in chimpanzees of antibodies inhibiting receptor-mediated cell fusion by HIV glycoprotein. Goudsmit, J., Smit, L., Klaver, B., Asher, D.M., Wolff, A., Gibbs, C.J., Gajdusek, D.C. Viral Immunol. (1987) [Pubmed]
  19. Insulin-Like Growth Factor-I Induces {alpha}1B-Adrenergic Receptor Phosphorylation through G{beta}{gamma} and Epidermal Growth Factor Receptor Transactivation. Molina-Mu??oz, T., Romero-Avila, M.T., Garc??a-S??inz, J.A. Mol. Endocrinol. (2006) [Pubmed]
  20. Characterization of the protease activity in the chemotactic factor inactivator. Ward, P.A., Ozols, J. J. Clin. Invest. (1976) [Pubmed]
  21. Mpe1, a zinc knuckle protein, is an essential component of yeast cleavage and polyadenylation factor required for the cleavage and polyadenylation of mRNA. Vo, L.T., Minet, M., Schmitter, J.M., Lacroute, F., Wyers, F. Mol. Cell. Biol. (2001) [Pubmed]
  22. Chemotactic factor inactivator interaction with Gc-globulin (vitamin D-binding protein). A mechanism of modulating the chemotactic activity of C5a. Robbins, R.A., Hamel, F.G. J. Immunol. (1990) [Pubmed]
  23. Is the development of myocardial tolerance to repeated ischemia in humans due to preconditioning or to collateral recruitment? Billinger, M., Fleisch, M., Eberli, F.R., Garachemani, A., Meier, B., Seiler, C. J. Am. Coll. Cardiol. (1999) [Pubmed]
  24. Insulin Growth Factor-I and Epidermal Growth Factor Receptors Recruit Distinct Upstream Signaling Molecules to Enhance AKT Activation in Mammary Epithelial Cells. Fleming, J.M., Desury, G., Polanco, T.A., Cohick, W.S. Endocrinology (2006) [Pubmed]
  25. Decreased chemotactic activity in activated newborn plasma. Tannous, R., Spitzer, R.E., Clarke, W.R., Goplerud, C.P., Cavendar-Zylich, N. J. Lab. Clin. Med. (1982) [Pubmed]
  26. Two distinct chemotactic factor inactivators in human serum. Till, G., Ward, P.A. J. Immunol. (1975) [Pubmed]
  27. Relationship between the C5 peptides chemotactic for leukocytes and tumor cells. Romualdez, A.G., Ward, P.A., Torikata, T. J. Immunol. (1976) [Pubmed]
  28. Transcriptional and post-transcriptional regulation of complement factor I (CFI) gene expression in Hep G2 cells by interleukin-6. Minta, J.O., Fung, M., Paramaswara, B. Biochim. Biophys. Acta (1998) [Pubmed]
  29. Alternative pathway complement activation in rheumatoid arthritis. El-Ghobarey, A., Whaley, K. J. Rheumatol. (1980) [Pubmed]
  30. Cleavage of the third complement component (C3) and generation of the spasmogenic peptide, C3a, in human serum via the properdin pathway: demonstration of inhibitory as well as enhancing effects of epsilon-amino-caproic acid. Vogt, W., Schmidt, G., Lynen, R., Dieminger, L. J. Immunol. (1975) [Pubmed]
  31. Genetic analysis of the complement factor H related 5 gene in haemolytic uraemic syndrome. Monteferrante, G., Brioschi, S., Caprioli, J., Pianetti, G., Bettinaglio, P., Bresin, E., Remuzzi, G., Noris, M. Mol. Immunol. (2007) [Pubmed]
  32. Physiologically assessed coronary collateral flow and intracoronary growth factor concentrations in patients with 1- to 3-vessel coronary artery disease. Fleisch, M., Billinger, M., Eberli, F.R., Garachemani, A.R., Meier, B., Seiler, C. Circulation (1999) [Pubmed]
  33. Alterations in activities of anaphylatoxin inactivator and chemotactic factor inactivator during hemodialysis. McCormick, J.R., Kreutzer, D.L., Keating, H.J., Hupp, J., Despins, A., Moore, M. Am. J. Pathol. (1982) [Pubmed]
  34. A novel oxalosuccinate-forming enzyme involved in the reductive carboxylation of 2-oxoglutarate in Hydrogenobacter thermophilus TK-6. Aoshima, M., Igarashi, Y. Mol. Microbiol. (2006) [Pubmed]
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