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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 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 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 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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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.
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.
A2E accumulation altered retinal microglial complement regulation by decreasing complement factor H (and increasing complement factor B (zeige CFB Antikörper) expression), favoring increased complement activation and lipofuscin deposition in the outer retina.
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.
C-reactive protein (zeige CRP Antikörper) amino acids 35-47 mediate the interaction with complement factor H in lupus nephritis
OCT (zeige Plxna2 Antikörper) scans revealed lower retinal thickness in patients homozygous for CFH or ARMS2 (zeige ARMS2 Antikörper), which was caused by a significantly reduced photoreceptor layer. The number and ultrastructure of drusen were also significantly different.
CFH rs1061170 has an important effect on age at onset of MDD in Han Chinese and may therefore be related to early pathogenesis of MDD.
Data suggest that disease-linked mutations in complement factor H (CFH) affect pivotal role of CFH in regulation of complement activation; mutations studied include those linked to atypical hemolytic uremic syndrome and age-related macular degeneration.
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