Anti-ABCG2 Polyclonal Antibody 2 is a Rabbit antibody targeting ABCG2. Anti-ABCG2 Polyclonal Antibody 2 can be used in ICC/IF,FCM.

IgG

Human (predicted:Mouse,Rat)

1. Blank control: A549.
Primary Antibody (green line): Rabbit Anti-ABCG2 antibody (TMAB-02163)
Dilution: 3 μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG.
Secondary Antibody: Goat anti-rabbit IgG-PE
Dilution: 3 μg /test.
Protocol
The cells were incubated in 5% BSA to block non-specific protein-protein interactions for 30 min at at room temperature. Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
2. Tissue/cell: A549 cell; 4% Paraformaldehyde-fixed; Triton X-100 at room temperature for 20 min; Blocking buffer (normal goat serum) at 37°C for 20 min; Antibody incubation with (ABCG2) polyclonal Antibody, Unconjugated (TMAB-02163) 1:100, 90 minutes at 37°C; followed by a FITC conjugated Goat Anti-Rabbit IgG antibody at 37°C for 90 minutes, DAPI (blue) was used to stain the cell nuclei.
3. HepG2 cell; 4% Paraformaldehyde-fixed; Triton X-100 at room temperature for 20 min; Blocking buffer (normal goat serum) at 37°C for 20 min; Antibody incubation with (ABCG2) polyclonal Antibody, Unconjugated (TMAB-02163) 1:100, 90 minutes at 37°C; followed by a conjugated Goat Anti-Rabbit IgG antibody at 37°C for 90 minutes, DAPI (blue) was used to stain the cell nuclei.

ICC/IF: 1:100-500; FCM: 3μg/Test

Polyclonal

KLH conjugated synthetic peptide: human ABCG2

Human

ABCG2

Broad substrate specificity ATP-binding cassette transporter ABCG2

Xenobiotic transporter that may play an important role in the exclusion of xenobiotics from the brain. May be involved in brain-to-blood efflux. Appears to play a major role in the multidrug resistance phenotype of several cancer cell lines. 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.