Human CFI ELISA Kit (V2LY-0626-LY3846)

Name: Human CFI ELISA Kit
SKU: V2LY-0626-LY3846
Rating: 5 (1 reviews)

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Tested Data

Datasheet

SDS

Request for COA

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

Basic Information

Sensitivity

1.42 ng/mL

Detection Range

3-900 ng/mL

Sample Type

Serum, Plasma, cell culture supernates

Specificity

Human

Assay Type

Sandwich

Reactivity

Human

Assay Time

1.5 h

Molecule Mass

65.8 kDa

Components

Pre-coated ELISA Plate: 12 wells * 8 detachable strips
Standard solution: 0.5ml x1
Standard diluent: 3ml x1
Streptavidin-HRP: 6ml x1
Stop solution: 6ml x1
Substrate solution A: 6ml x1
Substrate solution B: 6ml x1
Wash buffer concentrate (25x): 20ml x1
Biotinylated antibody: 1ml x1

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

Storage

Store at 2-8°C

More Infomation

Target

Full Name

Complement Factor I

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

Alternative Versions

Mouse Recombinant CFI protein, His Tag (CAT#: V2LY-0526-LY8290)

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Isotype control

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

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