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anti-Human Complement Factor H Anticorps:
anti-Mouse (Murine) Complement Factor H Anticorps:
anti-Rat (Rattus) Complement Factor H Anticorps:
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Human Monoclonal Complement Factor H Primary Antibody pour IP, ELISA - ABIN532648
Pangburn, Pangburn, Koistinen, Meri, Sharma: Molecular mechanisms of target recognition in an innate immune system: interactions among factor H, C3b, and target in the alternative pathway of human complement. dans Journal of immunology (Baltimore, Md. : 1950) 2000
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Human Monoclonal Complement Factor H Primary Antibody pour ELISA, WB - ABIN532661
Hourcade, Mitchell, Oglesby: A conserved element in the serine protease domain of complement factor B. dans The Journal of biological chemistry 1998
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Human Monoclonal Complement Factor H Primary Antibody pour IP, ELISA - ABIN2473069
Fontaine, Demares, Koistinen, Day, Davrinche, Sim, Ripoche: Truncated forms of human complement factor H. dans The Biochemical journal 1989
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Human Monoclonal Complement Factor H Primary Antibody pour IHC, ELISA - ABIN2192409
Oppermann, Baumgarten, Brandt, Gottsleben, Kurts, Götze: Quantitation of components of the alternative pathway of complement (APC) by enzyme-linked immunosorbent assays. dans Journal of immunological methods 1990
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Human Monoclonal Complement Factor H Primary Antibody pour ELISA, WB - ABIN2192411
Oppermann, Kurts, Zierz, Quentin, Weber, Götze: Elevated plasma levels of the immunosuppressive complement fragment Ba in renal failure. dans Kidney international 1992
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Human Polyclonal Complement Factor H Primary Antibody pour ELISA, WB - ABIN547483
Klein, Zeiss, Chew, Tsai, Sackler, Haynes, Henning, SanGiovanni, Mane, Mayne, Bracken, Ferris, Ott, Barnstable, Hoh: Complement factor H polymorphism in age-related macular degeneration. dans Science (New York, N.Y.) 2005
Human Polyclonal Complement Factor H Primary Antibody pour ID, WB - ABIN253380
Radu, Hu, Yuan, Welch, Makshanoff, Lloyd, McMullen, Travis, Bok: Complement system dysregulation and inflammation in the retinal pigment epithelium of a mouse model for Stargardt macular degeneration. dans The Journal of biological chemistry 2011
Human Monoclonal Complement Factor H Primary Antibody pour IHC (fro), FACS - ABIN2473067
Harrison, Lachmann: The physiological breakdown of the third component of human complement. dans Molecular immunology 1980
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The association of the SNP at the ARMS2/HTRA1 locus with subretinal/sub-RPE hemorrhage and poorer visual acuity and of SNPs at the CFH locus with drusen area may provide new insights in pathophysiological pathways underlying different stages of age-related macular degeneration.
Reports an association between a rare variant in the complement factor H-related 4 (CFHR4) gene and phenytoin-induced maculopapular exanthema in Europeans. This variant is in complete linkage disequilibrium with a missense variant (N1050Y) in the complement factor H (CFH) gene. In addition, results reinforce the association between HLA-A*31:01 and carbamazepine hypersensitivity.
findings suggested that both coding and noncoding variants in CFH acted synergistically to regulate the degree of complement activation and thereby contributed to immunoglobulin A nephropathy susceptibility.
The results indicate that augmented complement activation associated with advanced age-related macular degeneration could be attributed to a decrease in CFH activity in younger patients.
Crystal structures for the FH complexes with C3b and C3dg revealed that the extended N-terminal conformation accounted for C3b fluid-phase regulation.
Older age and the presence of CFH and ARMS2 risk alleles are two main risk factors associated with the prevalence of age-related macular degeneration in The Irish Longitudinal study on Ageing (TILDA) cohort.
Data show that complement factor H (FH) from patients with active anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV) exhibited a deficient ability in binding neutrophils and inhibiting ANCA-induced neutrophil activation in fluid phase and on endothelial cells.
The CFH Y402H polymorphism was associated with significantly increased membrane attack complex in RPE/choroid samples, but not in the serum, in a previously unstudied cohort with age related macular degeneration.
CFH rs1061170 is a significant genetic risk factor associated with choroidal thinning in normal eyes of the elderly population.
Hence, we demonstrate a functional consequence of the Y402H polymorphism in vivo, which promotes age-related macular degeneration (AMD)-like pathology development and affects lipoprotein levels in aged mice. These findings support targeting lipoproteins as a viable therapeutic strategy for treating AMD.
Complement factors in newly diagnosed Nigerian schizoprenic patients and those on antipsychotic therapy.
The presence of the risk allele of the Y402H polymorphism in the CFH gene was related to a less favorable evolution over 1 year in this sample of the Brazilian population with exudative AMD who were being treated with anti-VEGF drugs.
In our series of Italian patients, the CFHY402H genotype is associated with atrophic age-related macular degeneration (AMD) and retinitis pigmentosa (RP), but not with Stargardt disease (STGD). This result may support the hypothesis of a complement system dysregulation in the pathogenesis of AMD and RP.
Systemic Review/Meta-analysis: significant association between rs6677604-(A) allele and IgAN susceptibility, supporting the importance of complement activation in the pathogenesis of IgAN. The presence of rs6677604-(A) allele may be associated with a decreased the risk of IgAN in Europeans, but the association was not confirmed in Asians.
This study disclosed no difference in CRP levels per se between exudative AMD patients with control group. However, higher levels of CRP in the presence of C allele of Y402H might confer more risk for the development of exudative AMD.
the effect of the CFH rs1061170 polymorphism on age-related macular degeneration risk in ethnic groups (Meta-Analysis)
An Induced Pluripotent Stem Cell Patient Specific Model of Complement Factor H (Y402H) Polymorphism Displays Characteristic Features of Age-Related Macular Degeneration and Indicates a Beneficial Role for UV Light Exposure.
The Complement factor H (FH) contains mostly alpha2-6-linked sialic acid, making an intramolecular interaction with its alpha2-3-sialic acid specific binding site and an associated self-lock mechanism unlikely, substantiate that there is only a single sialic acid binding site in FH and none in FHL-1.
Factor H concentrations were higher in AKI patients
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
FH bound to the outer acrosomal region and soluble FH play important roles in protecting sperm against complement attack in male and female genital tracts.
our studies demonstrate a direct role of FH in the maintenance of bone structure and function and is highlighted as a promising therapeutic target in bone diseases.
The results demonstrate that factor H is important for limiting injury in the kidney after acute kidney ischemia/reperfusion injury, but it is not critical for controlling complement activation by immunoglobulin within the glomerulus in this setting.
this study shows that complement regulatory protein Factor H is a soluble prion receptor that potentiates peripheral prion pathogenesis
Factor H and Crry are critical for regulating complement activation at distinct anatomic sites within the kidney.
VEGF inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2/PKC-alpha/CREB signaling.
environmental factors can drive retinal disease in these mice when linked to complement deficits impairing immune function. Both groups of mice had similar levels of retinal amyloid beta accumulation. Consequently there is no direct link between this and inflammation in Cfh(-/-) mice.
role for serum FH levels in the host response to invasive pneumococcal infections
absence of plasma CfH conferred susceptibility to glomerulonephritis
This new understanding of the complicated interactions of CFH in AMD-like pathology provides an improved foundation for the development of targeted therapies for AMD
data suggest that altered interactions of Cfh with MDA-modified proteins may be relevant in explaining the effects of the Cfh variant.
Cfh and Cfhr2 genes are expressed in the mouse outer retina. Only Cfh mRNA was detected in the retinal pigment epithelium, but no protein.
A spectrum of complement dysregulation was modeled on the APOE4 age related macular degeneration mouse model by crossing these mice to complement factor H knockout (cfh-/-) mice to test the impact of excess complement activation.
Data indicate that co-deficiency of factor H (FH) and MASP-1/MASP-3 did not ameliorate either the plasma Complement C3 (C3) activation or glomerular C3 accumulation in FH-deficient mice.
A2E accumulation altered retinal microglial complement regulation by decreasing complement factor H (and increasing complement factor B expression), favoring increased complement activation and lipofuscin deposition in the outer retina.
endogenous fH makes a significant contribution to inhibition of the AP in CAIA through binding to sites of immune complex formation and complement activation.
The exaggerated humoral immune response in CFH(-/-) mice was normalized in CFH(-/-)C5aR(-/-) double knockout mice, highlighting the C5aR dependence.
Properdin deficiency exacerbated renal injury in mice lacking complement factor H.
nonsense mutations in SCR19 caused glomerulonephritis
IL-27 regulates complement activation through up-regulation of complement factor H in the retina.
interaction between sialylated Neisseria gonorrhoeae and factor H [factor H]
Results report the molecular cloning and identification of complement factor H and complement factor H-like 1-4 (CFHL1-4) in Danio rerio.
This gene is a member of the Regulator of Complement Activation (RCA) gene cluster and encodes a protein with twenty short consensus repeat (SCR) domains. This protein is secreted into the bloodstream and has an essential role in the regulation of complement activation, restricting this innate defense mechanism to microbial infections. Mutations in this gene have been associated with hemolytic-uremic syndrome (HUS) and chronic hypocomplementemic nephropathy. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
H factor 1 (complement)
, H factor 2 (complement)
, adrenomedullin binding protein
, age-related maculopathy susceptibility 1
, factor H
, factor H-like 1
, complement regulator factor H
, complement factor H
, complement factor H related protein 3A4/5G4
, protein beta-1-H
, complement component factor H
, complement inhibitory factor H
, platelet complement factor H
, complement factor H L homeolog