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Human Complement Factor H Kit ELISA pour Sandwich ELISA - ABIN365061
Shi, Zhao, Liu, Zhang, Zhou, Pu: Serum proteomics of methamphetamine addicts and up-regulation of complement factor H related to methamphetamine addiction. dans Neuroscience letters 2012
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Human Complement Factor H Kit ELISA pour Sandwich ELISA - ABIN414509
Lee, Park, Lee, Park, Shin, Park, Yoo, Cho, Kim, Kim, Namgoong, Lee, Lee, Cho, Han, Kang, Ha, Bae, Kim, Park, Cheong: Atypical hemolytic uremic syndrome: Korean pediatric series. dans Pediatrics international : official journal of the Japan Pediatric Society 2015
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Human Complement Factor H Kit ELISA pour Sandwich ELISA - ABIN511291
Lönnroth, Oshalim, Lange, Johansson: Interaction Of Proteasomes And Complement C3, Assay Of Antisecretory Factor In Blood. dans Journal of immunoassay & immunochemistry 2015
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 (Montrer ARMS2 Kits ELISA))/LOC387715 A69S (rs10490924) polymorphisms shown to have significant association with age-related macular degeneration (Meta-Analysis).
Regression analysis showed that ARMS2 (Montrer ARMS2 Kits ELISA) 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 (Montrer AMD1 Kits ELISA). We also revealed synergistic influence of CCL2 (Montrer CCL2 Kits ELISA)-2518 and the at-risk genotype of the C3 in AMD (Montrer AMD1 Kits ELISA) with an estimated AP = 50.9% (adjusted AP = 24.7%). Present findings show that CCL2 (Montrer CCL2 Kits ELISA)-2518 polymorphism is not an innocent bystander (Montrer SEPT1 Kits ELISA) in AMD (Montrer AMD1 Kits ELISA) 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 (Montrer CFHR3 Kits ELISA)/CFHR1 (Montrer CFHR1 Kits ELISA) 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 (Montrer ARMS2 Kits ELISA)/HTRA1 (Montrer HTRA1 Kits ELISA) genes play a major role in the genetic susceptibility to AMD (Montrer AMD1 Kits ELISA) in a Greek population. These findings are of direct relevance for disease and help mapping the genetic chart of AMD (Montrer AMD1 Kits ELISA).
Our results suggest the contribution of all four predicted CFH polymorphisms in age-related macular degeneration (AMD (Montrer AMD1 Kits ELISA)) susceptibility among the Iranian population. This association with CFH may lead to early detection and new strategies for prevention and treatment of AMD (Montrer AMD1 Kits ELISA).
Development of polypoidal choroidal vasculopathy (PCV) in the unaffected fellow eye is associated with ARMS2 (Montrer ARMS2 Kits ELISA) 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 (Montrer TGFB1 Kits ELISA) Factor H is a soluble prion (Montrer PRNP Kits ELISA) receptor that potentiates peripheral prion (Montrer PRNP Kits ELISA) pathogenesis
Factor H and Crry (Montrer CR1L Kits ELISA) are critical for regulating complement activation at distinct anatomic sites within the kidney.
VEGF (Montrer VEGFA Kits ELISA) inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2 (Montrer KDR Kits ELISA)/PKC-alpha (Montrer PKCa Kits ELISA)/CREB (Montrer CREB1 Kits ELISA) 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 (Montrer AMD1 Kits ELISA)-like pathology provides an improved foundation for the development of targeted therapies for AMD (Montrer AMD1 Kits ELISA)
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 (Montrer CFHR2 Kits ELISA) 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 (Montrer MASP1 Kits ELISA) did not ameliorate either the plasma Complement C3 (Montrer C3 Kits ELISA) (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 (Montrer CFHR1 Kits ELISA)-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