The BXP-9 Mab was selected after immunization with a fusion protein containing the E. coli maltose binding protein and a fragment of the mouse bcrp protein corresponding to amino acids 221-394. BXP-9 reacts with an internal epitope of bcrp, a 70 kD transmembrane half-transporter which is involved in Multidrug resistance. BXP-9 does not react with the human BCRP molecule.
Note: Not all species have been tested for usefulness with this product. Only those species listed have been tested. We cannot make any guarantees about additional reactivities which may or may not occur.
Synthetic peptide, corresponding to amino acids 221-394 of mouse BCRP/ABCG2 fused to maltose binding protein.
Localization:
Plasma membrane, integral membrane protein
Marker:
Hematopoietic Stem Cell Marker
Species Reactivity:
This antibody reacts with mouse. It does not react with human. Not yet tested in other species.
Applications:
Uses:
Immunocytochemistry: working dilution of 1:20 - 1:50 on acetone fixed cytospin preparations.
Dilutions:
Flow Cytometry, Immunocytochemistry 1:20, Immunohistochemistry-Frozen, Immunohistochemistry-Paraffin, Western Blot
Unit Size:
0.1 ml
Concentration:
This product is unpurified. Concentration is not relevant.
Packaging:
Storage:
Store at 4 °C short term. Aliquot and store at -20 °C long term. Avoid freeze-thaw cycles.
Buffer:
0.7% BSA (serum free)
Preservative:
0.1% Sodium Azide
Limitations:
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Products are guaranteed for 6 months from date of receipt, except for peptides and proteins which are guaranteed for 3 months.
An ABC transporter. Allows efflux of Hoechst dye, a property that has been used to separate bone marrow side population cells, which express BCRP/ABCG2. Appears to play a major role in the multidrug resistance phenotype of a specific MCF-7 breast cancer cell line. When overexpressed, the transfected cells become resistant to mitoxantrone, daunorubicin and doxorubicin, display diminished intracellular accumulation of daunorubicin, and manifest an ATP-dependent increase in the efflux of rhodamine 123.