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1 CFH quality and GC/GT practices for patients with breast
2 CFH(-/-).C3(-/-) mice had significantly more Abeta on Br
3 CFH, ARMS2, and C3 were associated with specific feature
4 CFH, secreted by many cell types, including those of the
5 CFH-deficient mice (CFH(-/-)) develop uncontrolled C3 ac
6 CFH/CFHR rearrangements were associated with poor clinic
11 ciated with a risk ratio (RR) of 1.83 with 2 CFH risk alleles (P = 1.03E-02), compared with outcomes
14 100 eyes of 51 patients with AMD carrying a CFH variant (mean [SD] age, 66.7 [12.1] years; 64.7% fem
15 complement-mediated hemolysis of ES PspCN, a CFH-binding Streptococcus pneumoniae protein domain, bin
16 support regarding the importance of accurate CFH and the benefits of proactive high-risk patient mana
17 a show that both uncontrolled C3 activation (CFH(-/-)) and complete absence of C3 (CFH(-/-).C3(-/-) a
18 ns across the region, including the adjacent CFH-related genes CFHR3 and CFHR1, which may themselves
19 These patients have autoantibodies against CFH domains 19 and 20 (CFH19-20), which are nearly ident
20 tors H and C3 (CFH(-/-).C3(-/-)), CFH alone (CFH(-/-)), or C3 alone (C3(-/-)), and wild-type mice (C5
24 , which remain significant in this analysis: CFH R1210C (OR = 18.82, P = 3.5 x 10-07), C3 K155Q (OR =
25 etic polymorphisms (CFH-402His [P = .04] and CFH-62Ile [P = .04]) and demographic factors (sex [P = .
28 viously identified associations of ARMS2 and CFH with type of choroidal neovascularization on fluores
29 ssociated with genetic variants in ARMS2 and CFH, indicating a genetic and pathophysiologic overlap b
30 e complement Factor H (CFH) gene cluster and CFH autoantibodies in six children with post-HSCT TMA.
31 s reported significantly less discomfort and CFH (P </= 0.02) and took a significantly lower dose of
33 action between glycosaminoglycans (GAGs) and CFH plays an important role in disease pathology of AMD.
34 onfirm that enhanced fucosylation of HPX and CFH may serve as an indicator of premalignant liver dise
37 24, HTRA1 SNPs rs11200638 and rs3793917, and CFH SNPs rs393955, rs1061170, and rs2274700 were associa
39 native pathway of the complement system, and CFH polymorphisms increase the genetic risk of age-relat
44 es and RPE cells carrying disease-associated CFH genetic variants had more alternative complement pat
46 fference between CFHR1 and the autoantigenic CFH epitope, suggesting a novel explanation for CFHR1 de
47 k score to determine the association between CFH risk and improvement in VA and central foveal thickn
49 reptococcus pneumoniae protein domain, binds CFH tightly and increases accessibility of CCPs 19 and 2
51 ssociation between genetic variation in both CFH and CFHR3 and susceptibility to meningococcal diseas
53 hs) mice deficient in both factors H and C3 (CFH(-/-).C3(-/-)), CFH alone (CFH(-/-)), or C3 alone (C3
54 ation (CFH(-/-)) and complete absence of C3 (CFH(-/-).C3(-/-) and C3(-/-)) negatively affect aged ret
55 in both factors H and C3 (CFH(-/-).C3(-/-)), CFH alone (CFH(-/-)), or C3 alone (C3(-/-)), and wild-ty
56 mice had plasma depleted of both C3 and C5, CFH(-/-).P(-/-) animals exhibited depletion of C3 predom
59 more, sera from carriers of the hybrid CFHR1/CFH gene induced more C5b-9 deposition on endothelial ce
60 found a duplication leading to a novel CFHR1/CFH hybrid gene in a family with two affected subjects.
61 serum of heterozygous carriers of the CFHR1/CFH hybrid gene indicated that the FHR1/FH hybrid protei
63 ntrolled activation of C3 driven by complete CFH deficiency, properdin influences the intraglomerular
68 , advanced age, high-fat diet, and decreased CFH induce sub-RPE deposit formation leading to compleme
70 ly, matching or outperforming plasma-derived CFH, whereas R53H-CFH, linked to atypical hemolytic urem
71 e interval [CI], 1.0-2.4) but not with donor CFH Y402H genotype (P = 0.626), after controlling for ag
74 interval [CI], 1.2-8.8) after adjustment for CFH genotype, anti-CMV IgG positivity, age, sex, and smo
75 ecreased with the number of risk alleles for CFH (P < .001), ARMS2 (P < .001), and C3 (P = .005).
78 s (25[OH]D <12 ng/mL) and 2 risk alleles for CFH Y402H (SI for additive interaction, 1.4; 95% CI, 1.1
81 ian FH serum levels were 299.4 microg/mL for CFH Arg175Gln and 266.3 microg/mL for CFH Ser193Leu carr
82 mL for CFH Arg175Gln and 266.3 microg/mL for CFH Ser193Leu carriers vs 302.4 and 283.0 microg/mL for
84 al. (2017) uncover a non-canonical role for CFH in the inhibition of mononuclear phagocyte eliminati
85 c expression was found to be significant for CFH, C3 and CFB, which are known risk genes for age-rela
87 single nucleotide polymorphisms in 7 genes (CFH, ARMS2/HTRA1, CFB, C2, C3, CFI, and LIPC) were genot
90 k was based on Y402H in complement factor H (CFH) and A69S in age-related maculopathy susceptibility
91 osome 1q32 contains the complement factor H (CFH) and five complement factor H-related (CFHR) genes.
92 variants in inhibitory complement factor H (CFH) are also features of both ARMD and TMA, we hypothes
93 Genetic variations in complement factor H (CFH) confer greater risk for age-related macular degener
94 Rare variants in the complement factor H (CFH) gene and their association with age-related macular
95 -coding variants in the complement factor H (CFH) gene are more strongly associated with age-related
96 netic variations in the complement Factor H (CFH) gene cluster and CFH autoantibodies in six children
97 02H risk variant in the complement factor H (CFH) gene developed neovascular AMD 2.8 (95% CI, 0.5-5.0
98 id position 402) in the complement factor H (CFH) gene have a pharmacogenetics effect on the anti-vas
99 e 1q31.1 containing the complement factor H (CFH) gene was strongly associated with serum MPO levels
100 ptibility 2 (ARMS2) and complement factor H (CFH) genotypes, and other factors, mean IMT was associat
107 of risk alleles of the complement factor H (CFH) or age-related maculopathy susceptibility 2 (ARMS2)
109 individuals with 1 or 2 complement factor H (CFH) risk alleles derived maximum benefit from antioxida
110 usceptibility genotypes Complement Factor H (CFH) RS1061170 and Age Related Maculopathy Susceptibilit
114 enetic loci in 7 genes [complement factor H (CFH), age-related maculopathy susceptibility 2/high-temp
115 or rare variants in the complement factor H (CFH), complement factor I (CFI), complement C9 (C9), and
117 the CFH gene, encoding complement factor H (CFH), show strong association with age-related macular d
118 ve complement regulator complement factor H (CFH), thereby inhibiting the alternative pathway of comp
120 of hemopexin (HPX) and complement factor H (CFH), two liver-secreted glycoproteins, in healthy indiv
121 status, presence of the complement factor H (CFH)-rs1061170 and age-related maculopathy susceptibilit
127 jury, plasma iron, and cell-free hemoglobin (CFH) levels depending on the age of stored blood (all, P
128 resh blood, which results in less hemolysis, CFH, and iron release, is less toxic than transfusion of
132 ial chromosomes expressing full-length human CFH variants and crossed these to Cfh knockout (Cfh(-/-)
135 lium/choroid/sclera, establishing that human CFH regulates activation of the mouse alternative pathwa
136 e created transgenic mouse lines using human CFH bacterial artificial chromosomes expressing full-len
139 versely, PspCN boosted the CA, on ES, of I62-CFH, R53H-CFH, and LA-CFH and also enhanced hemolysis pr
140 ichia pastoris We found that recombinant I62-CFH (protective against age-related macular degeneration
141 ry rare coding variants (frequency <0.1%) in CFH, CFI and TIMP3 suggest causal roles for these genes,
143 D may be protective for cCSC, and alleles in CFH that are protective for AMD confer risk for cCSC.
144 s the appearance of mesangial C3 deposits in CFH(-/-) mice; here, we show that these effects require
145 , or a higher degree of core fucosylation in CFH compared to HPX, but we did not identify changes dif
147 t that genotyping for the risk haplotypes in CFH and MCP may help predict the risk of developing aHUS
149 Only 8%-10% of patients with mutations in CFH, C3, or CFB had combined mutations, whereas approxim
151 y homozygous for rs10490924 and rs1061170 in CFH (OR, 62.3; 95% confidence interval, 16-242), with P
156 in known AMD risk-associated genes including CFH (rs800292, rs3766404, rs1061170, rs2274700 and rs393
159 the CA, on ES, of I62-CFH, R53H-CFH, and LA-CFH and also enhanced hemolysis protection by I62-CFH an
162 S-linked CCP 20 mutant S1191L/V1197A-CFH (LA-CFH) had dramatically reduced CA on ES but was less comp
163 strated that VEGF inhibition decreases local CFH and other complement regulators in the eye and kidne
166 l thickness overall, and subjects with a low CFH risk score improved more than the high-risk group.
168 its recognition of polyanions, which mediate CFH binding to host cell surfaces and extracellular matr
170 provement in VA was observed for the nonrisk CFH Y402H genotype (P < .001) and for a low CFH risk sco
171 h C3b degradation in carriers of CFI but not CFH variants, suggesting that CFH variants affect functi
174 s reviewed documented presence or absence of CFH in first-degree relatives, and 61.5% of medical reco
175 al records documented presence or absence of CFH in second-degree relatives, with significantly highe
176 smoking and presence of >/=1 risk allele of CFH-rs1061170 or ARMS2-rs10490924 were associated with l
177 d according to the number of risk alleles of CFH (rs1061170) or ARMS2 (rs10490924) as low (no or 1 ri
178 I, 1.3-3.2), and presence of risk alleles of CFH-rs1061170 (OR, 1.8; 95% CI, 1.3-2.4) or ARMS2-rs1049
179 sex and the presence of both risk alleles of CFH-rs1061170 or ARMS2-rs10490924 were independently ass
180 netic screening of aHUS includes analysis of CFH and CFHR rearrangements, particularly before a kidne
182 teins function as competitive antagonists of CFH to modulate complement activation in vivo and explai
183 the functional basis for the association of CFH and MPO variants with circulating MPO levels require
186 MP persistence arose secondary to binding of CFH to CD11b, which obstructed the homeostatic eliminati
188 ement and (2) analysis of the combination of CFH rs412852 and rs3766405 with ARMS2 c.372_815del443ins
190 oantigenic loop in the C-terminal domains of CFH and CFHR1, explaining the variation in binding of au
191 ntrary to expectation, electroretinograms of CFH(-/-).C3(-/-) mice displayed more severely reduced re
192 To mechanistically study the function of CFH in the pathogenesis of these diseases, we created tr
193 However, which of the several functions of CFH drives this self-surface selectivity remains unknown
194 rstanding of the complicated interactions of CFH in AMD-like pathology provides an improved foundatio
197 s, which express relatively higher levels of CFH, demonstrated functional and structural protection o
201 sit height, we interrogated the potential of CFH as a previously unidentified regulator of Bruch's me
205 Our data show that the CCP6-8 region of CFH binds more strongly to heparin (a highly sulfated fo
206 ange of structures, for which two regions of CFH (CCP6-8 and CCP19-20) have been implicated in HS bin
207 We examined the triangular relationships of CFH/CFHR3/CFHR1 genotype, plasma CFH or CFHR1 concentrat
210 core fucosylation at N882 and N911 sites of CFH, or a higher degree of core fucosylation in CFH comp
211 n fact, we demonstrate that gene variants of CFH and CFB, as well as demographic risk factors, confer
216 ionships of CFH/CFHR3/CFHR1 genotype, plasma CFH or CFHR1 concentrations and AMD susceptibility in co
219 H-raising rs6677604 allele and raised plasma CFH concentration were each associated with AMD protecti
223 e of progression with genetic polymorphisms (CFH-402His [P = .04] and CFH-62Ile [P = .04]) and demogr
224 show that hRPE cells of the AMD-predisposing CFH haplotype (HH402/VV62) are attacked by complement fo
226 n contrast, hRPE cells of the AMD-protective CFH haplotype (YY402/II62) showed no complement activati
227 spCN boosted the CA, on ES, of I62-CFH, R53H-CFH, and LA-CFH and also enhanced hemolysis protection b
228 tperforming plasma-derived CFH, whereas R53H-CFH, linked to atypical hemolytic uremic syndrome (aHUS)
231 patients, AMD was associated with recipient CFH Y402H genotype (P = 0.036; odds ratio [OR], 1.6; 95%
232 omplement attack, whereas cells with reduced CFH synthesis because of the Y402H and I62V substitution
233 f 212 practices completed measures regarding CFH and GC/GT practices for 10,466 patients; 77.4% of al
236 healthy lifestyle score (0-2) and high-risk CFH genotype (CC), relative to those who had low genetic
238 h low healthy lifestyle scores and high-risk CFH genotype were strengthened (odds ratio, 4.6; 95% CI,
241 ch patient was genotyped for SNPs rs1061170 (CFH), rs10490924 (ARMS2), rs11200638 (HTRA1), and rs2230
242 1 and were genotyped for the SNPs rs1061170 (CFH), rs10490924 (ARMS2),rs2230199 (C3), rs10468017 (LIP
243 involved 879 participants for whom the same CFH and ARMS2 single nucleotide polymorphisms were measu
247 using human Bruch's membrane explants, that CFH removes endogenous human lipoproteins in aged donors
249 of CFI but not CFH variants, suggesting that CFH variants affect functional activity of FH rather tha
254 and poorer visual acuity and of SNPs at the CFH locus with drusen area may provide new insights in p
256 ingle nucleotide polymorphisms (SNPs) at the CFH, FZD4, and HTRA1/ARMS2 loci were tested for replicat
258 we investigated the relationship between the CFH haplotype of human RPE (hRPE) cells, exposure to OS
259 here was a trend for association between the CFH Y402H T allele ("low risk" for AMD, n = 6) and impro
260 SNP rs6503905; P = 2.94 x 10(-12)), but the CFH locus did not exhibit evidence of association with p
262 ent advanced AMD among subjects carrying the CFH Y402H nonrisk (T) allele (P-trend = 0.0004, P-intera
263 um lipids, systemic and dietary factors, the CFH single nucleotide polymorphism (SNP) rs1061170 and A
264 vitamin D status and 2 risk alleles for the CFH and CFI genotypes, suggesting a synergistic effect b
268 iously described p.Arg1210Cys encoded in the CFH gene (case frequency (fcase) = 0.51%; control freque
269 ow that the common Y402H polymorphism in the CFH gene, associated with an increased risk of AMD, redu
276 e presence of at least 3 risk alleles of the CFH rs1061170 or ARMS2 rs10490924 genes (OR, 2.1; 95% CI
281 impairing complement regulation, whereas the CFH-411T polymorphism lacked functional consequences.
282 much less effective in AMD patients with the CFH CC genotype (CC versus TT: odds ratio (OR) = 55, 95%
283 rrent smokers at baseline, subjects with the CFH or ARMS2 risk genotypes, and pseudophakic eyes.
284 ide polymorphisms (SNPs) associated with the CFH, ARMS2, C3, LIPC, CFB, and C2 genes are associated w
285 ally, our data show that deposits are due to CFH competition for lipoprotein binding sites in Bruch's
289 The aHUS-linked CCP 20 mutant S1191L/V1197A-CFH (LA-CFH) had dramatically reduced CA on ES but was l
290 st age-related macular degeneration) and V62-CFH functioned equivalently, matching or outperforming p
292 rusen, carried essential splice site variant CFH 1:196648924 (IVS6+1G>A) or missense variant rs139360
293 etention of Sb (89-98%) in soil amended with CFH-12 (2%) mixed with limestone (1%) compared to unamen
296 e interactions, since genes interacting with CFH are retinal genes, and GO term enrichment also verif
297 and pack-years smoked and interactions with CFH and ARMS2 with the incidence and progression of AMD
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