Assay-kits

SensoLyte® Anti-Mouse MOG (1-125) IgG Quantitative ELISA Kit Colorimetric - 1 kit

443,00
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  • Cat.Number : AS-55156
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    In stock
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Mouse MOG recombinant protein (1-125) [Cat# AS-55150] is able to induces autoantibody production and relapsing-remitting neurological disease causing extensive plaque-like demyelination. Autoantibody response to mouse MOG (1-125) has been observed in induced experimental autoimmune encephalomyelitis (EAE) in C57/BL6, 129/Sv, B6, and SJL mice.
The SensoLyte® Anti-Mouse MOG (1-125) IgG Quantitative ELISA Kit provides a convenient quantitative assay for anti-mouse MOG (1-125) autoantibody. This colorimetric assay is useful to researchers for determining the amount of anti-mouse MOG (1-125) antibody present, and can help provide information on the role it plays in the development and treatment of EAE, an animal model for multiple sclerosis pathogenesis.

Specifications

Packaging
Kits components
  • Component A: Mouse MOG (1-125) coated and BSA blocked 8-well strips: 12 x 8 strips Component B: Anti-mouse MOG (1-125) IgG standard: 100 µl (20 µg/ml) Component C: 1X Sample Dilution Buffer: 30 ml Component D: 10X Wash Buffer: 50 ml Component E: TMB color substrate solution: 10 ml Component F: Stop Solution: 10 ml Component G: Secondary antibody, Goat anti-Mouse IgG-HRP: 30 µl
Chemistry
UniProt number
  • Q61885
Storage & stability
Storage Conditions
  • Store all kit components at 2-8°C for up to 6 months.
Activity
Application
Biomarker Target
Detection Method
Detection Limit
  • 1 ng/ml
Research Area
Sub-category Research Area
Usage
  • Research use
Codes
Code Nacres
  • NA.32

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Citations

MHC class II–dependent B cell APC function is required for induction of CNS autoimmunity independent of myelin-specific antibodies

J Exp Med . 2013 Dec 16 ; 210 2921 | DOI : 10.1084/jem.20130699

  • N. Molnarfi
  • et al

Substrain Differences Reveal Novel Disease-Modifying Gene Candidates That Alter the Clinical Course of a Rodent Model of Multiple Sclerosis

J Immunol . 2010 Feb 19 ; 184 3174 | DOI : 10.4049/jimmunol.0902881

  • L. Summers de Luca
  • et al