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anti-Human Complement Factor H Antikörper:
anti-Mouse (Murine) Complement Factor H Antikörper:
anti-Rat (Rattus) Complement Factor H Antikörper:
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Human Monoclonal Complement Factor H Primary Antibody für 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. in Journal of immunology (Baltimore, Md. : 1950) 2000
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Human Monoclonal Complement Factor H Primary Antibody für ELISA, WB - ABIN532661
Hourcade, Mitchell, Oglesby: A conserved element in the serine protease domain of complement factor B. in The Journal of biological chemistry 1998
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Human Monoclonal Complement Factor H Primary Antibody für IP, ELISA - ABIN2473069
Fontaine, Demares, Koistinen, Day, Davrinche, Sim, Ripoche: Truncated forms of human complement factor H. in The Biochemical journal 1989
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Human Monoclonal Complement Factor H Primary Antibody für IHC, ELISA - ABIN2192409
Oppermann, Baumgarten, Brandt, Gottsleben, Kurts, Götze: Quantitation of components of the alternative pathway of complement (APC) by enzyme-linked immunosorbent assays. in Journal of immunological methods 1990
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Human Monoclonal Complement Factor H Primary Antibody für ELISA, WB - ABIN2192411
Oppermann, Kurts, Zierz, Quentin, Weber, Götze: Elevated plasma levels of the immunosuppressive complement fragment Ba in renal failure. in Kidney international 1992
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Human Polyclonal Complement Factor H Primary Antibody für 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. in Science (New York, N.Y.) 2005
Human Polyclonal Complement Factor H Primary Antibody für 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. in The Journal of biological chemistry 2011
Human Monoclonal Complement Factor H Primary Antibody für IHC (fro), FACS - ABIN2473067
Harrison, Lachmann: The physiological breakdown of the third component of human complement. in Molecular immunology 1980
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Human Polyclonal Complement Factor H Primary Antibody für IF (p) - ABIN897170
Halder, Abdelfatah, Jo, Jacobsen, Westermann, Beyersdorf, Lorkowski, Zipfel, Skerka: Factor H Binds to Extracellular DNA Traps Released from Human Blood Monocytes in Response to Candida albicans. in Frontiers in immunology 2016
Complement factor H (CFH) is implied to play a role in tumor growth and metastasis. An autoantibody to CHF is associated with anti-tumor cell activity. The interaction of a human monoclonal antibody Ab42 that was isolated from a cancer patient with CFH polypeptide (pCFH) antigen was analyzed by molecular docking, molecular dynamics (MD) simulation.
The functional polymorphism rs3753394 in CFH gene was significantly correlated with susceptibility to sepsis due to P. aeruginosa infection in Chinese Han populations.
performed sequence analysis of the complement genes complement factor H (CFH), complement factor I (CFI), and complement C3 (C3) in 866 aHUS/C3G and 697 AMD patients. In total, we identified 505 low-frequency alleles, representing 121 unique variants, of which 51 are novel
In this GWAS on chronic central serous chorioretinopathy (cCSC), we identified a locus on chromosome 1 at the CFH gene that was significantly associated with cCSC, and we report protective and risk-conferring haplotypes in this gene.
Among patients with neovascular age-related macular degeneration (AMD), the AMD risk alleles ARMS2 and HTRA1 were associated with an increased risk of pseudodrusen and the risk allele CFH Y402H was associated with lower risk of pseudodrusen, supporting findings from previous studies.
This study demonstrate that variants of CFH that maximize complement activation are associated with a decreased risk of cognitive decline, a benefit which seems augmented by zinc supplementation.
data indicate that apoE and FH interact with monocytic cells in a concerted action and this interaction reduces complement activation and inflammation in the atherosclerotic lesions.
Oxidized CFH enhances Factor I mediated cleavage of C3 and C3b whereas the reduced form loses this activity in age-related macular degeneration.
Playing 'hide-and-seek' with factor H: game-theoretical analysis of a single nucleotide polymorphism.
The SNP rs3753396 in CFH and SNP rs6685931 in CFHR4 are associated with systemic complement activation levels. The SNP rs6685931 in CFHR4 and its linked haplotype H1-2 also conferred a risk for age-related macular degeneration (AMD) development, and therefore could be used to identify AMD patients who would benefit most from complement-inhibiting therapies.
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.
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.
the -1635 AP-1 motif on the CFH promoter region mediates Cd-inducible CFH gene expression
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
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