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Complement factor B

Complement Factor B, properdin factor B
This gene encodes complement factor B, a component of the alternative pathway of complement activation. Factor B circulates in the blood as a single chain polypeptide. Upon activation of the alternative pathway, it is cleaved by complement factor D yielding the noncatalytic chain Ba and the catalytic subunit Bb. The active subunit Bb is a serine protease which associates with C3b to form the alternative pathway C3 convertase. Bb is involved in the proliferation of preactivated B lymphocytes, while Ba inhibits their proliferation. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. This cluster includes several genes involved in regulation of the immune reaction. Polymorphisms in this gene are associated with a reduced risk of age-related macular degeneration. The polyadenylation site of this gene is 421 bp from the 5' end of the gene for complement component 2. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Properdin, AGE, HAD, CAN, ACID
Papers on Complement Factor B
Deficiency of the complement component 3 but not factor B aggravates Staphylococcus aureus septic arthritis in mice.
Jin et al., Göteborg, Sweden. In Infect Immun, Feb 2016
Mice lacking the complement component 3 (C3(-/-)), complement factor B (fB(-/-)), receptor for C3 derived anaphylatoxin C3a (C3aR(-/-)) and wild-type (WT) control mice were intravenously or intraarticularly inoculated with Staphylococcus aureus Newman strain.
Complement Factor B Production in Renal Tubular Cells and Its Role in Sodium Transporter Expression During Polymicrobial Sepsis.
Chao et al., Changsha, China. In Crit Care Med, Feb 2016
Complement factor B is essential for the alternative pathway of complement activation.
IL-6/STAT3 Plays a Regulatory Role in the Interaction Between Pancreatic Stellate Cells and Cancer Cells.
Shimosegawa et al., Sendai, Japan. In Dig Dis Sci, Feb 2016
Neutralization of IL-6 suppressed the PSC-CM-induced upregulation of genes including complement factor B, lipocalin, and chemokine (C-C motif) ligand 20.
Association of complement factor B allotypes and serum biomarkers in rheumatoid arthritis patients and their relatives.
Utiyama et al., Curitiba, Brazil. In Int J Immunogenet, Dec 2015
The aim of the study was to investigate the allotypic variability of complement factor B (BF) in patients and relatives with rheumatoid arthritis (RA) and its association with serological biomarkers and clinical features of the disease.
Adherence to a Mediterranean diet, genetic susceptibility, and progression to advanced macular degeneration: a prospective cohort study.
Seddon et al., Boston, United States. In Am J Clin Nutr, Nov 2015
Ten genetic loci in 7 genes [complement factor H (CFH), age-related maculopathy susceptibility 2/high-temperature requirement A serine peptidase 1 (ARMS2/HTRA1), complement component 2 (C2), complement factor B (CFB), complement component 3 (C3), collagen type VIII α 1 (COL8A1), and RAD51 paralog B (RAD51B)] were examined.
Structural insights on complement activation.
Llorca et al., Madrid, Spain. In Febs J, Oct 2015
The displacement of the thio-ester-containing domain (TED) exposes hidden surfaces that mediate the interaction with complement factor B to assemble the C3-convertase of the alternative pathway (AP).
[Atypical HUS caused by complement-related abnormalities].
Matsumoto et al., Nara, Japan. In Rinsho Ketsueki, Feb 2015
Many aHUS cases (approximately 70%) are reportedly caused by uncontrolled complement activation due to genetic mutations in the alternative pathway, including complement factor H (CFH), complement factor I (CFI), membrane cofactor protein (MCP), thrombomodulin (THBD), complement component C3 (C3), and complement factor B (CFB).
[The genetic variability of complement system in pathogenesis of age-related macular degeneration].
Sanak et al., In Klin Oczna, 2014
Recently, variants in several genes, such as complement H (CFH), complement factor B (CFB), complement 2 (C2), and complement 3 (C3), encoding complement pathway proteins, have been identified as associated with age-related macular degeneration.
The association between complement component 2/complement factor B polymorphisms and age-related macular degeneration: a HuGE review and meta-analysis.
Attia et al., Bangkok, Thailand. In Am J Epidemiol, 2012
This meta-analysis provides evidence for an association between C2/CFB polymorphisms and age-related macular degeneration.
Prepregnancy obesity and complement system activation in early pregnancy and the subsequent development of preeclampsia.
Holers et al., Aurora, United States. In Am J Obstet Gynecol, 2012
Women who were obese with levels of Bb or C3a in the top quartile were 10.0 (95% confidence interval, 3.3-30) and 8.8 (95% confidence interval, 3-24) times, respectively, more likely to develop preeclampsia compared with the referent group.
Complement activation in patients with isolated antiphospholipid antibodies or primary antiphospholipid syndrome.
Hunt et al., London, United Kingdom. In Thromb Haemost, 2012
significantly increased levels in patients with antiphospholipid antibodies or primary antiphospholipid syndrome
Association of polymorphisms in C2, CFB and C3 with exudative age-related macular degeneration in a Korean population.
Chin et al., Inch'ŏn, South Korea. In Exp Eye Res, 2012
In conclusion, the genetic effect of C2, CFB and C3 polymorphisms, which are known to be important for AMD in Caucasian, were not significant in the Korean population.
Association of C2 and CFB polymorphisms with anterior uveitis.
Pang et al., Hong Kong, Hong Kong. In Invest Ophthalmol Vis Sci, 2011
Our results revealed an association between Anterior uveitis and Complement Factor B-rs1048709.
Atypical Hemolytic-Uremic Syndrome
Remuzzi et al., Seattle, United States. In Unknown Journal, 2007
The genes: CFH (encoding complement factor H and accounting for ~30% of aHUS; CD46 (MCP) (encoding membrane cofactor protein and accounting for ~12% of aHUS); CFI (encoding complement factor I; ~5%-10% of aHUS), C3 (encoding the third component of complement C3; ~5% of aHUS); CFB (encoding complement factor B; rare); THBD (encoding thrombomodulin; ~3%-5% of aHUS); DGKE (encoding diacylglycerol kinase; ~27% of aHUS manifesting before age 1 year) .
Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H.
Botto et al., London, United Kingdom. In Nat Genet, 2002
Introducing a second mutation in the gene encoding complement factor B, which prevents C3 turnover in vivo, obviates the phenotype of Cfh(-/-) mice.
Adipsin and complement factor D activity: an immune-related defect in obesity.
Spiegelman et al., Boston, United States. In Science, 1989
Activated adipsin has little or no proteolytic activity toward most substrates but has the same activity as human complement factor D, cleaving complement factor B when it is complexed with activated complement component C3.
Regulation of class III major histocompatibility complex gene products by interleukin-1.
Colten et al., In Science, 1986
One of two structurally and functionally homologous major histocompatibility complex (MHC) class III genes encodes a positive acute-phase protein, complement factor B. The closely linked complement C2 gene is not affected during the acute-phase response.
Structure of the human interleukin-2 receptor gene.
Greene et al., In Science, 1985
Exons 2 and 4 were derived from a gene duplication event and unexpectedly also are homologous to the recognition domain of human complement factor B. Alternative messenger RNA (mRNA) splicing may delete exon 4 sequences, resulting in a mRNA that does not encode a functional IL-2 receptor.
Close genetic linkage between diabetes mellitus and kidd blood group.
Rotter et al., In Lancet, 1981
Under three different genetic models for IDDM, evidence was found for linkage between the disease and two distinct sets of marker loci: three markers on chromosome 6 (HLA, properdin factor B, and glyoxalase-1), and the Kidd blood group locus.
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