Mouse Anti-CFI Recombinant Antibody (CBFYC-1765) (CBMAB-C1827-FY)

Name: Mouse Anti-CFI Recombinant Antibody (CBFYC-1765)
SKU: CBMAB-C1827-FY
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBFYC-1765

Application

WB, FC, ELISA, IP

Immunogen

Human complement Factor I.

Host Species

Mouse

Specificity

Human

Antibody Isotype

IgG1

Clonality

Monoclonal Antibody

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
ELISA	1:40,000
FC	1 µg/10^6 cells

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS

Preservative

0.02% sodium azide

Concentration

1 mg/ml

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.

Epitope

AA 19-118

More Infomation

Target

Full Name

Complement Factor I

Introduction

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 uremic syndrome, a disease characterized by acute renal failure, microangiopathic hemolytic anemia and thrombocytopenia. Primary glomerulonephritis with immune deposits and age-related macular degeneration are other conditions associated with mutations of this gene.

Entrez Gene ID

3426

UniProt ID

P05156

Alternative Names

Complement Factor I; Konglutinogen-Activating Factor; C3B/C4B Inactivator; C3b-Inactivator; IF; Complement Control Protein Factor I; Complement Factor I Heavy Chain; Light Chain Of Factor I; Complement Component I; I Factor (Complement)

Function

Trypsin-like serine protease that plays an essential role in regulating the immune response by controlling all complement pathways. Inhibits these pathways by cleaving three peptide bonds in the alpha-chain of C3b and two bonds in the alpha-chain of C4b thereby inactivating these proteins (PubMed:7360115, PubMed:17320177).
Essential cofactors for these reactions include factor H and C4BP in the fluid phase and membrane cofactor protein/CD46 and CR1 on cell surfaces (PubMed:2141838, PubMed:9605165, PubMed:12055245).
The presence of these cofactors on healthy cells allows degradation of deposited C3b by CFI in order to prevent undesired complement activation, while in apoptotic cells or microbes, the absence of such cofactors leads to C3b-mediated complement activation and subsequent opsonization (PubMed:28671664).

Biological Process

Complement activation, classical pathway Source: UniProtKB-KW
Innate immune response Source: UniProtKB-KW
Regulation of complement activation Source: Reactome
Viral process Source: UniProtKB-KW

Cellular Location

Extracellular space; Secreted

Involvement in disease

Hemolytic uremic syndrome atypical 3 (AHUS3): An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease.
Complement factor I deficiency (CFI deficiency): Autosomal recessive condition associated with a propensity to pyogenic infections.
Macular degeneration, age-related, 13 (ARMD13): A form of age-related macular degeneration, a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.

Jia, B. B., Jin, C. D., & Li, M. F. (2020). The trypsin-like serine protease domain of Paralichthys olivaceus complement factor I regulates complement activation and inhibits bacterial growth. Fish & shellfish immunology, 97, 18-26.

Hallam, T. M., Marchbank, K. J., Harris, C. L., Osmond, C., Shuttleworth, V. G., Griffiths, H., ... & Lotery, A. J. (2020). Rare genetic variants in complement factor I lead to low FI plasma levels resulting in increased risk of age-related macular degeneration. Investigative ophthalmology & visual science, 61(6), 18-18.

Lv, W., Ma, A., Chi, X., Li, Q., Pang, Y., & Su, P. (2020). A novel complement factor I involving in the complement system immune response from Lampetra morii. Fish & shellfish immunology, 98, 988-994.

Altmann, T., Torvell, M., Owens, S., Mitra, D., Sheerin, N. S., Morgan, B. P., ... & Forsyth, R. (2020). Complement factor I deficiency: A potentially treatable cause of fulminant cerebral inflammation. Neurology-Neuroimmunology Neuroinflammation, 7(3).

Yu, Q., Zhu, J., Yao, Y., & Sun, C. (2020). Complement family member CFI polymorphisms and AMD susceptibility from a comprehensive analysis. Bioscience reports, 40(4), BSR20200406.

Shields, A. M., Pagnamenta, A. T., Pollard, A. J., Taylor, J. C., Allroggen, H., Patel, S. Y., ... & Smith, C. (2019). Classical and non-classical presentations of complement factor I deficiency: two contrasting cases diagnosed via genetic and genomic methods. Frontiers in immunology, 10, 1150.

Tseng, M. H., Lin, S. H., Wu, C. Y., Chien, H. P., Yang, H. Y., Chen, Y. C., ... & Huang, J. L. (2018). Serum complement factor I is associated with disease activity of systemic lupus erythematosus. Oncotarget, 9(9), 8502.

Lashkari, K., Teague, G., Chen, H., Lin, Y. Q., Kumar, S., McLaughlin, M. M., & López, F. J. (2018). A monoclonal antibody targeting amyloid β (Aβ) restores complement factor I bioactivity: Potential implications in age-related macular degeneration and Alzheimer’s disease. PLoS One, 13(5), e0195751.

Nanthapisal, S., Eleftheriou, D., Gilmour, K., Leone, V., Ramnath, R., Omoyinmi, E., ... & Brogan, P. A. (2018). Cutaneous vasculitis and recurrent infection caused by deficiency in complement factor I. Frontiers in immunology, 9, 735.

Franco-Jarava, C., de la Campa, E. Á., Solanich, X., Morandeira-Rego, F., Mas-Bosch, V., García-Prat, M., ... & Colobran, R. (2017). Early versus late diagnosis of complement factor I deficiency: clinical consequences illustrated in two families with novel homozygous CFI mutations. Journal of clinical immunology, 37(8), 781-789.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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For research use only. Not intended for any clinical use.

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