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Mutation in CFH gene is associated with age-related macular degeneration.
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 (zeige VEGFA Proteine) treatment, while patients with TT rs1061170 CFH genotype showed better functional and structural response to anti-VEGF (zeige VEGFA Proteine) agents.
Our analysis showed stronger contribution of ARMS2 (zeige ARMS2 Proteine) in age-related macular degeneration (AMD (zeige AMD1 Proteine)) with reticular pseudodrusen (RPD) group versus AMD (zeige AMD1 Proteine) without RPD group, in comparison with CFH genotypes.
Study demonstrated that a novel complotype composed of CFB (zeige CFB Proteine) (rs4151667) in combination with CFB (zeige CFB Proteine) (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 (zeige AMD1 Proteine).
AMD (zeige AMD1 Proteine) patients had significantly elevated nitrated CFH levels compared to controls (p = 0.0117). These findings strongly suggest that nitrated CFH contributes to AMD (zeige AMD1 Proteine) 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 (zeige ARMS2 Proteine))/LOC387715 A69S (rs10490924) polymorphisms shown to have significant association with age-related macular degeneration (Meta-Analysis).
Regression analysis showed that ARMS2 (zeige ARMS2 Proteine) 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 (zeige AMD1 Proteine). We also revealed synergistic influence of CCL2 (zeige CCL2 Proteine)-2518 and the at-risk genotype of the C3 in AMD (zeige AMD1 Proteine) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (zeige CCL2 Proteine)-2518 polymorphism is not an innocent bystander (zeige SEPT1 Proteine) in AMD (zeige AMD1 Proteine) susceptibility when combined with the at-risk genotype of C3 (R102G).
this study shows that complement regulatory protein (zeige TGFB1 Proteine) Factor H is a soluble prion (zeige PRNP Proteine) receptor that potentiates peripheral prion (zeige PRNP Proteine) pathogenesis
Factor H and Crry (zeige CR1L Proteine) are critical for regulating complement activation at distinct anatomic sites within the kidney.
VEGF (zeige VEGFA Proteine) inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2 (zeige KDR Proteine)/PKC-alpha (zeige PKCa Proteine)/CREB (zeige CREB1 Proteine) 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 (zeige AMD1 Proteine)-like pathology provides an improved foundation for the development of targeted therapies for AMD (zeige AMD1 Proteine)
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 (zeige CFHR2 Proteine) 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 (zeige MASP1 Proteine) did not ameliorate either the plasma Complement C3 (zeige C3 Proteine) (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 (zeige CFHR1 Proteine)-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