More info
Assay Range | 15.6-1,000 pg/mL |
Sensitivity | 10.0 pg/mL |
Size | 96T |
Storage | Store at 2 - 8ºC. Keep reconstituted standard and detection Ab at -20 ºC |
Assay Principle | Sandwich ELISA |
Sample Volume | 100 µL final volume, dilution factor varies on samples |
Detection Method | Chromogenic |
Kit Components
1. Recombinant Human MIA standard: 2 vials
2. One 96-well plate coated with anti-Human MIA Ab
3. Sample diluent buffer: 12 mL - 1
4. Detection antibody: 130 µL, dilution 1:100
5. Streptavidin-HRP: 130 µL, dilution 1:100
6. Antibody diluent buffer: 12 mL x1
7. Streptavidin-HRP diluent buffer: 12 mL x1
8. TMB developing agent: 10 mL x1
9. Stop solution: 10 mL x1.
10. Washing solution (20x): 25 mL x1.
Background
Melanoma Inhibiting Activity (MIA), also known as cartilage-derived retinoic acid-sensitive protein (CD-RAP), Melanoma-derived growth regulatory protein, or Melanoma inhibitory activity protein, is a secreted protein belonging to the MIA/OTOR family which is characteristic of one SH3 domain in their primary structure. MIA is widely expressed in developing and regenerating cartilage and in endodermal epithelium and parenchyma of developing lungs. Mature human MIA shares 90% and 92% amino acid sequence identity with mouse and rat MIA, respectively.
MIA disrupts cellular interactions with the extracellular matrix by binding to Integrins α4β1 and α5β1. It competes with Fibronectin fragments for Integrin binding and interferes with Integrin signaling. This polarization reduces cellular attachment to the matrix at the trailing pole and contributes to directional tumor cell migration. It has been showed that MIA is upregulated in several cancers including malignant melanoma, lung adenoma, metastatic oral squamous cell carcinoma, neurofibromatosis type 1 (NF-1)-related tumors, and pancreatic cancer. MIA inhibits tumor cell proliferation and cell-cell contact while enhancing migration and invasion. MIA functions as a chemoattractant for mesenchymal stem cells and enhances their BMP-2 and TGF-β3 induced differentiation into chondrocytes. It is reported that MIA-deficient mice exhibit delayed chondrocyte differentiation but enhanced chondrocyte proliferation and cartilage repair.