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Human Monoclonal Complement Factor H Primary Antibody for 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 Polyclonal Complement Factor H Primary Antibody for ELISA, WB - ABIN250548
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 Monoclonal Complement Factor H Primary Antibody for 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 for 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
Our analysis showed stronger contribution of ARMS2 (show ARMS2 Antibodies) in age-related macular degeneration (AMD (show AMD1 Antibodies)) with reticular pseudodrusen (RPD) group versus AMD (show AMD1 Antibodies) without RPD group, in comparison with CFH genotypes.
Study demonstrated that a novel complotype composed of CFB (show CFB Antibodies) (rs4151667) in combination with CFB (show CFB Antibodies) (rs641153) and CFH(rs800292) is strongly associated with complement activation and age-related macular degeneration status.
Mapping rare, deleterious mutations in Factor H: Association with early onset, drusen burden, and lower antigenic levels in familial AMD (show AMD1 Antibodies).
AMD (show AMD1 Antibodies) patients had significantly elevated nitrated CFH levels compared to controls (p = 0.0117). These findings strongly suggest that nitrated CFH contributes to AMD (show AMD1 Antibodies) 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 (show ARMS2 Antibodies))/LOC387715 A69S (rs10490924) polymorphisms shown to have significant association with age-related macular degeneration (Meta-Analysis).
Regression analysis showed that ARMS2 (show ARMS2 Antibodies) 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 (show AMD1 Antibodies). We also revealed synergistic influence of CCL2 (show CCL2 Antibodies)-2518 and the at-risk genotype of the C3 in AMD (show AMD1 Antibodies) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (show CCL2 Antibodies)-2518 polymorphism is not an innocent bystander (show SEPT1 Antibodies) in AMD (show AMD1 Antibodies) 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.
To our knowledge, this is the first evaluation of the involvement of the CFHR3 (show CFHR3 Antibodies)/CFHR1 (show CFHR1 Antibodies) deletion and age-related macular degeneration in CFH Y402H polymorphism Brazilian patients.
this study shows that complement regulatory protein (show TGFB1 Antibodies) Factor H is a soluble prion (show PRNP Antibodies) receptor that potentiates peripheral prion (show PRNP Antibodies) pathogenesis
Factor H and Crry (show CR1L Antibodies) are critical for regulating complement activation at distinct anatomic sites within the kidney.
VEGF (show VEGFA Antibodies) inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2 (show KDR Antibodies)/PKC-alpha (show PKCa Antibodies)/CREB (show CREB1 Antibodies) 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.
absence of plasma CfH conferred susceptibility to glomerulonephritis
This new understanding of the complicated interactions of CFH in AMD (show AMD1 Antibodies)-like pathology provides an improved foundation for the development of targeted therapies for AMD (show AMD1 Antibodies)
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 (show CFHR2 Antibodies) 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 (show MASP1 Antibodies) did not ameliorate either the plasma Complement C3 (show C3 Antibodies) (C3) activation or glomerular C3 accumulation in FH-deficient mice.
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 (show CFHR1 Antibodies)-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