Anti-Bcl-2 alpha Polyclonal Antibody is a Rabbit antibody targeting Bcl-2 alpha. Anti-Bcl-2 alpha Polyclonal Antibody can be used in WB,IHC-P,IHC-Fr,IF,FCM.

IgG

Human (predicted:Dog,Pig,Cow,Horse,Rabbit,Sheep)

1. Tissue/cell: Human kidney tissue; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer (0.01 M, pH 6.0), Boiling bathing for 15 min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30 min; Blocking buffer (normal goat serum) at 37℃ for 20 min;
Incubation: Anti-Bcl-2 Polyclonal Antibody, Unconjugated (TMAB-03049) 1: 200, overnight at 4°C, followed by conjugation to the secondary antibody and DAB staining
2. Blank control: HL-60.
Primary Antibody (green line): Rabbit Anti-Bcl-2 alpha antibody (TMAB-03049)
Dilution: 1 μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG.
Secondary Antibody: Goat anti-rabbit IgG-AF488
Dilution: 1 μg /test.
Protocol
The cells were fixed with 4% PFA (10 min at room temperature) and then permeabilized with 0.1%PBST for 20 min at room temperature. The cells were then incubated in 5% BSA to block non-specific protein-protein interactions for 30 min 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.
3. Sample:
Lane 1: Recombinant human Bcl-2 protein, C-His
Primary: Anti-Bcl-2 alpha (TMAB-03049) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 26 kDa
Observed band size: 26 kDa

WB: 1:500-2000; IHC-P: 1:100-500; IHC-Fr: 1:100-500; IF: 1:100-500; FCM: 1μg/Test

Polyclonal

KLH conjugated synthetic peptide: human Bcl-2 alpha

Human

BCL2

Apoptosis regulator Bcl-2

Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).