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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Complement factor I

CFI, Complement Factor I, C3b inactivator, Complement component, C3bINA
This gene encodes a serine proteinase that is essential for regulating the complement cascade. The encoded preproprotein is cleaved to produce both heavy and light chains, which are linked by disulfide bonds to form a heterodimeric glycoprotein. This heterodimer can cleave and inactivate the complement components C4b and C3b, and it prevents the assembly of the C3 and C5 convertase enzymes. Defects in this gene cause complement factor I deficiency, an autosomal recessive disease associated with a susceptibility to pyogenic infections. Mutations in this gene have been associated with a predisposition to atypical hemolytic uraemic syndrome, a disease characterized by acute renal failure, microangiopathic hemolytic anemia and thrombocytopenia. Primary glomerulonephritis with immmune deposits is another condition associated with mutation of this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, AGE, Complement Factor H, ACID
Papers on CFI
Rare Genetic Variants Associated With Development of Age-Related Macular Degeneration.
den Hollander et al., Nijmegen, Netherlands. In Jama Ophthalmol, Feb 2016
Importance: Rare variants in the complement genes CFH, CFI, C9, and C3 have been found to be highly associated with age-related macular degeneration (AMD); however, the effect on clinical characteristics and familial segregation by these variants is lacking.
In vitro and clinical evaluation of SIG1273: a cosmetic functional ingredient with a broad spectrum of anti-aging and antioxidant activities.
Pérez et al., Princeton, United States. In J Cosmet Dermatol, Feb 2016
Since then, they have been developed as novel cosmetic functional ingredients (CFI) and topical drug candidates.
Functional single nucleotide polymorphism in IL-17A 3' untranslated region is targeted by miR-4480 in vitro and may be associated with age-related macular degeneration.
Tuo et al., Bethesda, United States. In Environ Mol Mutagen, Jan 2016
Genetic factors contributing to AMD include single nucleotide polymorphisms (SNPs) in immune-related genes including CFH, C2, CFI, C9, and C3, thus implicating these pathways in AMD pathogenesis.
Complement Component 3 Is Regulated by TWIST1 and Mediates Epithelial-Mesenchymal Transition.
Afshar-Kharghan et al., Houston, United States. In J Immunol, Jan 2016
UNASSIGNED: We have previously shown that complement component 3 (C3) is secreted by malignant epithelial cells.
A large genome-wide association study of age-related macular degeneration highlights contributions of rare and common variants.
Heid et al., Ann Arbor, United States. In Nat Genet, Jan 2016
Very rare coding variants (frequency <0.1%) in CFH, CFI and TIMP3 suggest causal roles for these genes, as does a splice variant in SLC16A8.
Age-related macular degeneration: Complement in action.
Yaspan et al., San Francisco, United States. In Immunobiology, Jan 2016
Polymorphisms in genes encoding two important negative regulators of the alternative complement pathway, complement factor H (CFH) and complement factor I (CFI), are associated with the risk for Age-Related Macular Degeneration (AMD), a leading cause of vision impairment in the ageing population.
Identification of novel gene and pathway targets for human epilepsy treatment.
Wei et al., Jilin, China. In Biol Res, Dec 2015
In down-co-expression module, C1QB (complement C1s), C1S (complement component 1, S subcomponent) and CFI (complement factor I) were enriched in GO:0006955 ~ immune response.
Targeting Polo-Like Kinases: A Promising Therapeutic Approach for Cancer Treatment.
Liu, West Lafayette, United States. In Transl Oncol, Jun 2015
Other Plk inhibitors, including the Plk1 inhibitors GSK461364A, TKM-080301, GW843682, purpurogallin, and poloxin and the Plk4 inhibitor CFI-400945 fumarate, are in earlier clinical development.
Discovery of orally active anticancer candidate CFI-400945 derived from biologically promising spirooxindoles: success and challenges.
Liu et al., Zhengzhou, China. In Eur J Med Chem, Jun 2015
Among spirooxindoles, CFI-400945 holds its promise as the first potent PLK4 inhibitor, the fumarate of CFI-400945 has entered phase I clinical trials for the treatment of solid tumors.
[Atypical HUS caused by complement-related abnormalities].
Matsumoto et al., Nara, Japan. In Rinsho Ketsueki, Feb 2015
Many aHUS cases (approximately 70%) are reportedly caused by uncontrolled complement activation due to genetic mutations in the alternative pathway, including complement factor H (CFH), complement factor I (CFI), membrane cofactor protein (MCP), thrombomodulin (THBD), complement component C3 (C3), and complement factor B (CFB).
Functional characterization of CFI-400945, a Polo-like kinase 4 inhibitor, as a potential anticancer agent.
Mak et al., Toronto, Canada. In Cancer Cell, 2014
A drug discovery program culminated in CFI-400945, a potent and selective PLK4 inhibitor.
Polo-like kinase 4 inhibition: a strategy for cancer therapy?
Cleveland et al., Baltimore, United States. In Cancer Cell, 2014
In this issue of Cancer Cell, Mason and colleagues describe the development of a Polo-like kinase 4 (PLK4) inhibitor (CFI-400945), with promising activity against tumors formed in mice from patient-derived tumor tissue.
Rare variants in CFI, C3 and C9 are associated with high risk of advanced age-related macular degeneration.
Raychaudhuri et al., Boston, United States. In Nat Genet, 2013
We found that 7.8% of AMD cases compared to 2.3% of controls are carriers of rare missense CFI variants (odds ratio (OR) = 3.6; P = 2 × 10(-8)).
A functional variant in the CFI gene confers a high risk of age-related macular degeneration.
den Hollander et al., Nijmegen, Netherlands. In Nat Genet, 2013
Here, we report the identification of a rare, highly penetrant missense mutation in CFI encoding a p.Gly119Arg substitution that confers high risk of AMD (P = 3.79 × 10⁻⁶; odds ratio (OR) = 22.20, 95% confidence interval (CI) = 2.98-164.49).
Analysis of binding sites on complement factor I using artificial N-linked glycosylation.
Blom et al., Malmö, Sweden. In J Biol Chem, 2012
all analyzed cofactors form similar trimolecular complexes with FI and C3b/C4b, and the accessibility of FIMAC and SP domains is crucial for the function of FI
Early complementopathy after multiple injuries in humans.
Huber-Lang et al., Ulm, Germany. In Shock, 2012
factor I were significantly diminished early after trauma.
Factor I autoantibodies in patients with atypical hemolytic uremic syndrome: disease-associated or an epiphenomenon?
Marchbank et al., Newcastle upon Tyne, United Kingdom. In Clin J Am Soc Nephrol, 2012
Results question whether complement factor I autoantibodies per se predispose to atypical hemolytic uremic syndrome.
Acquisition of complement inhibitor serine protease factor I and its cofactors C4b-binding protein and factor H by Prevotella intermedia.
Blom et al., Malmö, Sweden. In Plos One, 2011
Since FI requires cofactors for its activity we also investigated the binding of purified cofactors C4BP and FH and found acquisition of both proteins, which retained their activity in FI mediated degradation of C3b and C4b.
Genetic factors for choroidal neovascularization associated with high myopia.
Seddon et al., Créteil, France. In Invest Ophthalmol Vis Sci, 2011
One SNP (rs10033900) in the CFI gene, which encodes a protein involved in the inflammatory pathway, was significantly associated with myopic choroidal neovascularization in multivariate analysis after correction for multiple testing.
Protective molecules and their cognate antibodies: new players in autoimmunity.
Doria et al., Padova, Italy. In Auto Immun Highlights, 2010
Complement component C1q, Creactive protein (CRP), serum amyloid P (SAP), mannose-binding lectin (MBL), apolipoprotein A-1 (Apo A-1) and long pentraxin 3 (PTX3) are molecules involved in the removal of apoptotic bodies and pathogens, and in other antiinflammatory pathways.
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