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

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Basic Information

Expressed Host
HEK293 Cells
Protein Species
Mouse
Tag
His Tag
Protein Construction
This product is Mouse Recombinant CFI protein, His Tag consist of Amino Acid: 1-603 and predicts a molecular mass of 66.75 kDa.
Molecule Mass
66.75 kDa
Verified
HPLC
Sequence
Amino Acid: 1-603
Species
Mouse

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

Purity
≥95% as determined by SDS-PAGE. ≥90% as determined by SEC-HPLC.
Endotoxin
Please contact us for more information.
Format
Lyophilized
Reconstitution
Allow the vial and reconstitution buffer to equilibrate to room temperature. Briefly centrifuge or tap down the vial to ensure that all lyophilized powder is collected at the bottom of the vial. For the reconstitution of this product, we recommend adding PBS or sterile water to achieve a final antibody concentration of 1 mg/mL. Allow the vial to reconstitute for 10-15 minutes at room temperature with gentle agitation. Avoid vigorous shaking that can cause foaming and antibody denaturation. Aliquot into volumes based on your experiment and store liquid protein at -20°C or -80°C for long time.
Buffer
Lyophilized from sterile Tirs, NaCl, Glycerol
Preservative
None
Storage
Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
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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For research use only. Not intended for any clinical use.

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