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Human Polyclonal Complement Factor B Primary Antibody for IHC, IHC (p) - ABIN4299962
Singh, Kapoun, Higgins, Kutschke, Thurman, Zhang, Singh, Yang, Guan, Lowe, Weiss, Zimmermann, Yull, Blackwell, Mohler, Anderson: Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heart. in The Journal of clinical investigation 2009
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Human Polyclonal Complement Factor B Primary Antibody for IHC, IHC (p) - ABIN4299963
Kato, Nicholson, Neiman, Rantalainen, Holmes, Barrett, Uhlén, Nilsson, Spector, Schwenk: Variance decomposition of protein profiles from antibody arrays using a longitudinal twin model. in Proteome science 2011
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Human Monoclonal Complement Factor B Primary Antibody for IHC (fro), FACS - ABIN2473065
Sulser: [The rhabdomyosarcoma with regard to age, sex, localization, pathological anatomy, and prognosis (author's transl)]. in Virchows Archiv. A, Pathological anatomy and histology 1978
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Human Monoclonal Complement Factor B Primary Antibody for Func, IHC (fro) - ABIN2473064
Xu, Narayana, Volanakis: Structural biology of the alternative pathway convertase. in Immunological reviews 2001
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Study demonstrated that a novel complotype composed of CFB (rs4151667) in combination with CFB (rs641153) and CFH (show CFH Antibodies)(rs800292) is strongly associated with complement activation and age-related macular degeneration status.
target sequencing of age-related macular degeneration (AMD (show AMD1 Antibodies)) susceptibility genes identified enrichment of low-frequency coding variants in CETP (show CETP Antibodies), C2 and CFB are associated with AMD (show AMD1 Antibodies) susceptibility in the Japanese population
Heterozygous variants in the CFB gene can be pathogenic and associated with immune-complex diffuse membranoproliferative glomerulonephritis and atypical hemolytic uremic syndrome
The complement activation factors Bb, C3a, C5a, and MAC were increased significantly in early-onset severe pre-eclampsia (EOSPE) (all P<.01) and late-onset severe pre-eclampsia (LOSPE). (P value: .027, <.001, .001, and <.001, respectively) compared with E/L-control. C1q and C4d were increased significantly in LOSPE (P value: .003 and .014, respectively) compared with L-control.
These results suggest (i) apparent allelic heterogeneity in CFB and genetic heterogeneity in SLC44A4 (show SLC44A4 Antibodies) across different ethnic groups; (ii) shared ulcerative colitis genetic etiological factors among Asians
Neutralization of the complement factor C3-dependent antichlamydial activity was dependent on the proteolytic activity of Chlamydia trachomatis CPAF and correlated with the CPAF-mediated degradation of complement factor C3 and factor B (show ATP5S Antibodies).
Our results revealed a significant association of CFB with non-infectious uveitis, particularly predisposed to VKH disease. Genetic differences for uveitis could be gender-specific.
There is a link between phenotype BF SS07 and allotype BF*S07 with aCl-IgM in systemic lupus erythematosus patients; BF*F allotype could be considered a marker of protection against the development of antiphospholipid antibodies in these patients.
CFB is downregulated in non-small cell lung cancer patients compared to those with benign lung disease or no lung disease.
individuals with the chronic hepatitis B (CHB) risk genotype CC of rs12614 had significantly lower CFB concentrations than those carrying one or two rs12614 T alleles (CT or TT carriers) both in normal populations and CHB patients
CfB plays a crucial role in late-phase of adipocyte differentiation and subsequent lipid droplet formation.
AP inhibitors not only prevent, but have the potential to accelerate the clearance of complement-mediated ocular injury. Improving our understanding of the regulation of the AP is paramount to developing novel treatment approaches for AMD (show AMD1 Antibodies).
The roles of C3, CfB, and C3a (show C3 Antibodies) receptor in the severity of S. aureus induced septic arthritis are reported.
Study shows that Factor B regulates UVA and UVB induced immunosuppression, UV induced edema and mast cell infiltration into the skin
Mouse RPE (show RPE Antibodies) cells express and secrete CFB sufficient to promote RPE (show RPE Antibodies) damage and CNV.
Properdin-deficient mice developed less severe collagen-antibody-induced arthritis than did wild-type mice.
Properdin provides protection from Citrobacter rodentium-induced intestinal inflammation in a C5a/IL-6 (show IL6 Antibodies)-dependent manner.
A2E accumulation altered retinal microglial complement regulation by increasing complement factor B (and decreasing complement factor H (show CFH Antibodies) expression), favoring increased complement activation and lipofuscin deposition in the outer retina.
study found that Streptococcus pneumoniae induced increased gene expression of factor B of the alternative complement pathway and C3 in mouse middle ear epithelium
TLR4 (show TLR4 Antibodies) stimulation or activation of RNA-sensing mechanisms results in synthesis and release of factor B by macrophages through distinct but overlapping mechanisms
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.
, C3 proaccelerator
, C3 proactivator
, C3/C5 convertase
, glycine-rich beta glycoprotein
, glycine-rich beta-glycoprotein
, properdin factor B
, complement component factor B
, complement factor B
, complement component 2
, complement factor Bf-1
, Factor B
, alternative-complement pathway C3/C5 convertase
, complement component 2 (within H-2S)
, histocompatibility 2, complement component factor B