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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 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 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 IHC (fro), FACS - ABIN2473067
Harrison, Lachmann: The physiological breakdown of the third component of human complement. dans Molecular immunology 1980
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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
factors other than the CFH Y402H polymorphism may be involved in the progression of neovascular age-related macular degeneration after treatment with anti-VEGF agents, in Malaysian population
Functional characterization of disease-associated genetic variants in the complement factor H gene in atypical hemolytic uremic syndrome and C3-glomerulopathy patients.
Evasion of C3b deposition at division septa and lateral amplification underneath the capsule requires localization of the FH-binding protein PspC at division sites.
These findings reveal that the CRP- and PTX3-binding characteristics of FHL-1 differ from those of FH, likely underpinning independent immune regulatory functions in the context of the human retina.
Two rare age-related macular degeneration-associated variants in the CFH gene (rs121913059 [p.Arg1210Cys] and rs35292876) deviate in frequency among different geographic regions.
these data demonstrate that Mesenchymal Stem Cells inhibit the activation of pathogenic C5 via up-regulation of FH, which improves our understanding of the immunomodulatory mechanisms of MSCs in the treatment of lupus nephritis.
Mutation in CFH gene is associated with age-related macular degeneration.
antioxidant and zinc nutritional supplement modifies risk of macular degeneration progression according to genotype
CC rs1061170 CFH genotype may be associated with the age-related macular degeneration. Additionally, CC rs1061170 CFH genotype may promote a negative response to anti-VEGF treatment, while patients with TT rs1061170 CFH genotype showed better functional and structural response to anti-VEGF agents.
Our analysis showed stronger contribution of ARMS2 in age-related macular degeneration (AMD) with reticular pseudodrusen (RPD) group versus AMD without RPD group, in comparison with CFH genotypes.
in Chinese lupus nephritis patients, the variants in the FH gene might affect the histopathologic subtypes and some clinical features of the disease
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.
The rs193053835 single nucleotide polymorphism showed the most significant protective effect to be associated with susceptibility to Meningococcal disease.
Mapping rare, deleterious mutations in Factor H: Association with early onset, drusen burden, and lower antigenic levels in familial AMD.
AMD patients had significantly elevated nitrated CFH levels compared to controls (p = 0.0117). These findings strongly suggest that nitrated CFH contributes to AMD progression, and is a target for therapeutic intervention.
inhibition of the alternative pathway by factor H, with a concentration equivalent to a high physiological level, strongly reduced C5a levels and decreased proinflammatory cytokine production in human peripheral blood mononuclear cells.
Complement factor H Y402H (rs1061170) and age-related maculopathy susceptibility2 (ARMS2)/LOC387715 A69S (rs10490924) polymorphisms shown to have significant association with age-related macular degeneration (Meta-Analysis).
Regression analysis showed that ARMS2 TT genotype has a statistically significant effect on retinal angiomatous proliferation versus age-related macular degeneration compared to CFH genotypes (P < 0.001).
This study enclosed strong synergistic association of risk genotypes of C3 and CFH Y402H with AMD. We also revealed synergistic influence of CCL2-2518 and the at-risk genotype of the C3 in AMD with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2-2518 polymorphism is not an innocent bystander in AMD susceptibility when combined with the at-risk genotype of C3 (R102G).
Our results suggest that factor H can interfere with mycobacterial entry into macrophages and modulate inflammatory cytokine responses, particularly during the initial stages of infection, thus affecting the extracellular survival of the pathogen.
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.
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.
While the connection between CFH deficiency and failure to upregulate CD59a remains unknown, these results suggest that expression of CD59 is tissue-specific and that neuroretinal regulation depends on CFH.
CFH influences age-related macular degeneration risk by modulating oxidative stress, inflammation, and abnormal angiogenesis
Although endogenous factor H (fH) limits the development of allergen-induced airway hyperresponsiveness and airway inflammation, the protection afforded by fH is incomplete.
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