| Species |
Human |
| Protein Construction |
Integrin alpha 2B beta 3 (ITGA2B&ITGB3) Heterodimer [Leu32-Arg993(ITGA2B) acidic tail & GLy27-Asp718(ITGB3) basic tail]
Accession # P08514-1(ITGA2B)&P05106-1(ITGB3) |
His |
| N-term |
C-term |
|
| Purity |
> 95% as determined by BisTris PAGE
> 95% as determined by HPLC |
| Endotoxin Level |
Less than 1EU per μg by the LAL method. |
| Biological Activity |
Measured by its binding ability in a functional ELISA. Immobilized Abciximab at 1μg/ml (100μl/well) on the plate can bind Integrin alpha 2B beta 3 (ITGA2B&ITGB3) Heterodimer, His, Human. Test result was comparable to standard batch. |
| Expression System |
HEK293 |
| Theoretical Molecular Weight |
110.5 kDa (ITGA2B)&81.3 kDa (ITGB3) |
| Apparent Molecular Weight |
Due to glycosylation, the protein migrates to 95-115 kDa based on Bis-Tris PAGE result. |
| Formulation |
Lyophilized from 0.22μm filtered solution in PBS (pH 7.4). |
| Reconstitution |
Centrifuge the tube before opening. Reconstituting to a concentration more than 100 μg/ml is recommended. Dissolve the lyophilized protein in distilled water. |
| Storage & Stability |
Upon receiving, the product remains stable up to 6 months at -20 °C or below. Upon reconstitution, the product should be stable for 3 months at -80 °C. Avoid repeated freeze-thaw cycles. |
| Target Background |
Glanzmann thrombasthenia (GT) is characterized by mucocutaneous bleeding due to platelets that fail to aggregate in response to physiologic stimuli. GT, a rare inherited disease, is caused by quantitative or qualitative deficiencies of αIIbβ3, an integrin receptor for adhesive proteins. Coded by the ITGA2B and ITGB3 genes, αIIbβ3 mediates platelet-to-platelet attachment, aggregation and clot retraction. |
| Synonyms |
α2Bβ3; ITGA2B&ITGB3; ITGA2B; ITGB3 |
For research use only. Not intended for human or animal clinical trials, therapeutic or diagnostic use.
