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anti-Human Complement Factor B Antibodies:
anti-Mouse (Murine) Complement Factor B Antibodies:
anti-Rat (Rattus) Complement Factor B Antibodies:
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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 Func, IHC (fro) - ABIN2473064
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 IHC (fro), FACS - ABIN2473065
Xu, Narayana, Volanakis: Structural biology of the alternative pathway convertase. in Immunological reviews 2001
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The pooled ORs for rs551397, rs2274700, rs4151667, rs641153, rs1047286, rs9332739, and rs547154 in the heterozygote model were 0.53, 0.53 , 0.54, 0.48, 1.42, 0.50, and 0.52, respectively. We confirmed the protective role of C2/CFB/CFH polymorphisms in the development of Age-Related Macular Degeneration (AMD), and showed single nucleotide polymorphism in C3 was a high-risk factor for AMD
Study demonstrated that a novel complotype composed of CFB (rs4151667) in combination with CFB (rs641153) and CFH(rs800292) is strongly associated with complement activation and age-related macular degeneration status.
target sequencing of age-related macular degeneration (AMD) susceptibility genes identified enrichment of low-frequency coding variants in CETP, C2 and CFB are associated with AMD 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 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.
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.
The Relationship of Longitudinal Levels of Complement Bb During Pregnancy with Preeclampsia
P serum level expression could be a reliable clinical biomarker to identify patients with underlying surface alternative pathway C5 convertase dysregulation.
CFB is downregulated in non-small cell lung cancer patients compared to those with benign lung disease or no lung disease.
These results suggest that a maternal immune response through complement fB might play a role in the development of preeclampsia, particularly in African-American patients.
mutation results in atypical hemolytic uremic syndrome
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
Complement factor B is a novel biomarker candidate for pancreatic ductal adenocarcinoma.
complement factor B has an important role in the etiology of familial C3 glomerulonephritis
A mutation in complement factor B was associated with a case of C3 glomerulonephritis.
The C2 and CFB gene variants were shown to be associated with polypoidal CNV. Typical PCV was not associated with variants in these genes.
Complement factor B is potently upregulated locally in inflammatory bowel disease in addition to having a possible central role in systemic complement activation.
These data suggest that properdin insufficiency promotes a tumour environment that helps the tumour evade the immune response
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.
The roles of C3, CfB, and C3a 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 cells express and secrete CFB sufficient to promote RPE 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-dependent manner.
role in the pathogenesis of severe bacterial sepsis
A2E accumulation altered retinal microglial complement regulation by increasing complement factor B (and decreasing complement factor H 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 stimulation or activation of RNA-sensing mechanisms results in synthesis and release of factor B by macrophages through distinct but overlapping mechanisms
Study identified novel mutations in CFH, CFHR5, CFI, CFB and C3 in American patients with atypical hemolytic uremic syndrome.
Bacterial titers of both Streptococcus pneumoniae serotype 6A and 14 in the middle ear lavage fluid samples from Bf/C2(-/)(-), Bf(-)(/)(-), and C1qa(-/)(-) mice were significantly higher than in samples from wild-type mice.
Administration of an estrogenic steroid to immature or ovariectomized adult mice markedly stimulated the expression of Bf, C3, and their RNA messages in the endometrium
Factor B-deficient mice are highly resistant to collagen-induced arthritis and display a decreased type II collagen-specific IgG antibody response, which can be boosted by repeated immunization.
The region between -556 and -282 bp of the the BF promoter mediates TNF-alpha responsiveness as well as the synergistic effect of TNF-alpha and IFN-gamma on BF promoter activation in macrophages.
critical role of complement factor B and viral evasion of complement in acute, persistent, and latent gamma-herpesvirus infection
Bf-deficient mice develop substantially less functional and morphologic renal injury following ischemia/reperfusion, with virtually no tubulointerstitial deposition of C3 or neutrophil infiltration in the outer medulla.
Factor B of the alternative complement pathway regulates development of airway hyperresponsiveness and inflammation
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