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Our analysis showed stronger contribution of ARMS2 (show ARMS2 Proteins) in age-related macular degeneration (AMD (show AMD1 Proteins)) with reticular pseudodrusen (RPD) group versus AMD (show AMD1 Proteins) without RPD group, in comparison with CFH genotypes.
Study demonstrated that a novel complotype composed of CFB (show CFB Proteins) (rs4151667) in combination with CFB (show CFB Proteins) (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 Proteins).
AMD (show AMD1 Proteins) 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 Proteins) 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 Proteins))/LOC387715 A69S (rs10490924) polymorphisms shown to have significant association with age-related macular degeneration (Meta-Analysis).
Regression analysis showed that ARMS2 (show ARMS2 Proteins) 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 Proteins). We also revealed synergistic influence of CCL2 (show CCL2 Proteins)-2518 and the at-risk genotype of the C3 in AMD (show AMD1 Proteins) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (show CCL2 Proteins)-2518 polymorphism is not an innocent bystander (show SEPT1 Proteins) in AMD (show AMD1 Proteins) 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 Proteins)/CFHR1 (show CFHR1 Proteins) deletion and age-related macular degeneration in CFH Y402H polymorphism Brazilian patients.
this study shows that complement regulatory protein (show TGFB1 Proteins) Factor H is a soluble prion (show PRNP Proteins) receptor that potentiates peripheral prion (show PRNP Proteins) pathogenesis
Factor H and Crry (show CR1L Proteins) are critical for regulating complement activation at distinct anatomic sites within the kidney.
VEGF (show VEGFA Proteins) inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2 (show KDR Proteins)/PKC-alpha (show PKCa Proteins)/CREB (show CREB1 Proteins) 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 Proteins)-like pathology provides an improved foundation for the development of targeted therapies for AMD (show AMD1 Proteins)
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 Proteins) 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 Proteins) did not ameliorate either the plasma Complement C3 (show C3 Proteins) (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 Proteins)-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