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These results suggest (i) apparent allelic heterogeneity in CFB and genetic heterogeneity in SLC44A4 (zeige SLC44A4 Proteine) 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 (zeige ATP5S Proteine).
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
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.
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 (zeige AMD1 Proteine).
The roles of C3, CfB, and C3a (zeige C3 Proteine) 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 (zeige RPE Proteine) cells express and secrete CFB sufficient to promote RPE (zeige RPE Proteine) 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 (zeige IL6 Proteine)-dependent manner.
A2E accumulation altered retinal microglial complement regulation by increasing complement factor B (and decreasing complement factor H (zeige CFH Proteine) 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 (zeige TLR4 Proteine) 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 (zeige CFH Proteine), CFHR5 (zeige CFHR5 Proteine), CFI (zeige CFI Proteine), CFB and C3 in American patients with atypical hemolytic uremic syndrome.
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.
complement component factor B
, complement factor B
, complement component 2
, complement factor Bf-1
, ATP synthase subunit s, mitochondrial
, ATP synthase, H+ transporting, mitochondrial F0 complex, subunit s (factor B)
, ATP synthase-coupling factor B
, Factor B
, mitochondrial ATP synthase regulatory component factor B
, B-factor, properdin
, C3 proaccelerator
, C3 proactivator
, C3/C5 convertase
, glycine-rich beta glycoprotein
, glycine-rich beta-glycoprotein
, properdin factor B
, alternative-complement pathway C3/C5 convertase
, complement component 2 (within H-2S)
, histocompatibility 2, complement component factor B