Intended Use
The Mouse Sm IgG Antibody ELISA Kit is designed for the Semi-quantitative analysis of Mouse Serum, plasma samples.
Contents of Kit
1. Polystyrene microwell ELISA plates coated with a purified antigen(12-1 x 8 wells), with holder in foil package containing desiccants
2. Negative Control, 1 vial of buffer 1.2 mL
3. Positive Control, 1 vial of buffer 1.2 mL
4. Calibrator A, 1 vial of buffer containing preservative, prediluted, 1.2 mL
5. Calibrator B, 1 vial of buffer containing preservative, prediluted, 1.2 mL
6. Calibrator C, 1 vial of buffer containing preservative, prediluted, 1.2 mL
7. Calibrator D, 1 vial of buffer containing preservative, prediluted, 1.2 mL
8. Sample Diluent, 1 vial – colored straw containing PBS-buffered saline, protein stabilizers and preservative, 50 mL.
9. Antibody Enzyme Conjugate, colored blue containing buffer, protein stabilizers and preservative, 12 mL
10. Wash Buffer (20 ×), 50 mL
11. TMB Chromogen, containing stabilizers, 10 mL
12. Stop Solution, Colorless, 10 mL
Storage
2–8 °C, protected from light and moisture.
Detection Range
0 - 200 U
General Description
Antibodies reactive with autologous nuclear components, such as DNA and histones, can represent an autoim mune basis for pathological conditions such as systemic lupus erythematosis (SLE) in humans. In mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr ), a systemic autoim munity develops with age which includes elevated levels of anti-dsDNA and other anti-nuclear antibodies (ANA), including anti-Sm (Smith antigen), a non-histone nuclear protein associated with ribonucleoprotein particles and having a role in post-translational pre-messenger RNA processing.
The expanded use in the drug industry of biological modifiers has been associated with production of autoantibodies, of which mice, and possibly also other hosts such as humans and monkeys, are susceptible. A prototype disease in mice is lupus caused by the drug minocycline, with elevated anti-dsDNA among other autoantibodies and pathological conditions.
Recent investigations have focused on the role of innate im mune mechanisms, including Toll-like receptors (TLRs) and TH2 im munity, responding to the damage-associated molecular patterns of dying cells, as underlying cause of autoim munity; these may be induced by drugs, including vaccines and adjuvants, with aging, or with other health conditions.
Citations
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