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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 - 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 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 Polyclonal Complement Factor H Primary Antibody für 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 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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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 Antikörper))/LOC387715 A69S (rs10490924) polymorphisms shown to have significant association with age-related macular degeneration (Meta-Analysis).
Regression analysis showed that ARMS2 (zeige ARMS2 Antikörper) 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 Antikörper). We also revealed synergistic influence of CCL2 (zeige CCL2 Antikörper)-2518 and the at-risk genotype of the C3 in AMD (zeige AMD1 Antikörper) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (zeige CCL2 Antikörper)-2518 polymorphism is not an innocent bystander (zeige SEPT1 Antikörper) in AMD (zeige AMD1 Antikörper) 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 (zeige CFHR3 Antikörper)/CFHR1 (zeige CFHR1 Antikörper) deletion and age-related macular degeneration in CFH Y402H polymorphism Brazilian patients.
The findings of the present study provide evidence that CFH gene variants and ARMS2 (zeige ARMS2 Antikörper)/HTRA1 (zeige HTRA1 Antikörper) genes play a major role in the genetic susceptibility to AMD (zeige AMD1 Antikörper) in a Greek population. These findings are of direct relevance for disease and help mapping the genetic chart of AMD (zeige AMD1 Antikörper).
Our results suggest the contribution of all four predicted CFH polymorphisms in age-related macular degeneration (AMD (zeige AMD1 Antikörper)) susceptibility among the Iranian population. This association with CFH may lead to early detection and new strategies for prevention and treatment of AMD (zeige AMD1 Antikörper).
Development of polypoidal choroidal vasculopathy (PCV) in the unaffected fellow eye is associated with ARMS2 (zeige ARMS2 Antikörper) A69S genotype in patients with unilateral PCV.
Identification of rare CFH variant carriers may be important for upcoming complement-inhibiting therapies. Patients with an extensive drusen area, drusen with crystalline appearance, and drusen nasal to the optic disc are more likely to have a rare variant in the CFH gene.
this study shows that complement regulatory protein (zeige TGFB1 Antikörper) Factor H is a soluble prion (zeige PRNP Antikörper) receptor that potentiates peripheral prion (zeige PRNP Antikörper) pathogenesis
Factor H and Crry (zeige CR1L Antikörper) are critical for regulating complement activation at distinct anatomic sites within the kidney.
VEGF (zeige VEGFA Antikörper) inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2 (zeige KDR Antikörper)/PKC-alpha (zeige PKCa Antikörper)/CREB (zeige CREB1 Antikörper) 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 Antikörper)-like pathology provides an improved foundation for the development of targeted therapies for AMD (zeige AMD1 Antikörper)
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 Antikörper) 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 Antikörper) did not ameliorate either the plasma Complement C3 (zeige C3 Antikörper) (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 Antikörper)-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