|Application ||WB, IHC-F, E, Func|
|Calculated MW||65750 Da|
|Purification||Purified IgG prepared by affinity chromatography on Protein A|
|Immunogen||Native human factor I from serum.|
|Shelf Life||18 months from date of despatch.|
|Other Names||Complement factor I, 126.96.36.199, C3B/C4B inactivator, Complement factor I heavy chain, Complement factor I light chain, CFI, IF|
|Target/Specificity||Mouse anti-Human Complement Factor I antibody, clone 3R/8 recognizes complement factor I, a member of the peptidase S1 family present in the blood plasma. Factor I is an 88 kDa protein consisting of one polypeptide chain of 35.4 kDa and one of 27.6 kDa. Factor I is a serine protease which inactivates complement components C3b and C4b. C3b cleavage requires the presence of cofactors complement component (3b/4b) receptor 1 (CR1), membrane cofactor protein or factor H, while C4b cleavage requires complement component 4 binding protein or CR1. Factor I has no natural inhibitors.Dysfunctional factor I can lead to uncontrolled activation of the alternative complement pathway causing in systemic depletion of C3 and lower levels of factors B and H, resulting in recurrent pyogenic infections. Defects in CFI are also associated with haemolytic uraemic syndrome.Mouse anti-Human Complement Factor I antibody, clone 3R/8 blocks function of complement factor I.Removal of Sodium Azide is recommended prior to use in functional assays. AbD Serotec recommend the use of EQU003 for this purpose.|
|Preservative & Stabilisers||0.09% Sodium Azide|
|Storage||Store at +4℃ or at -20 ℃.|
|Precautions||Anti-Human Complement Factor I Antibody, clone 3R/8 is for research use only and not for use in diagnostic or therapeutic procedures.|
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Provided below are standard protocols that you may find useful for product applications.
1. Dragon-Durey, M.V. et al. (2005) Atypical haemolytic uraemic syndrome and mutations in complement regulator genes. Springer Semin Immunopathol. 27:359-374. 2. Nilsson, S. et al. (2007) A mutation in factor I that is associated with atypical hemolytic uremic syndrome does not affect the function of factor I in complement regulation. Mol. Immunol. 44:1835-1844.
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