Product Description
Bax Antibody [SPM336] | 34-157 | ProSci
Host: Mouse
Reactivity: Human, Monkey,
Homology: N/A
Immunogen: Amino acids 3-16 (GSGEQPRGGGPTSS) from the human protein were used as the immunogen for this anti-Bax antibody.
Research Area: Apoptosis, Autophagy, Cancer
Tested Application: Flow, IF, WB, IHC
Application: Flow Cytometry: 0.5-1 ug/million cells in 0.1ml
Immunofluorescence: 1-2 ug/ml
Western blot: 0.5-1 ug/ml
Immunohistochemistry (FFPE) : 0.5-1 ug/ml for 30 minutes at RT (1)
Prediluted format : incubate for 30 min at RT (2)
The optimal dilution of the anti-Bax antibody for each application should be determined by the researcher.
1. Staining of formalin-fixed tissues requires boiling tissue sections in 10mM Tris with 1mM EDTA, pH 9.0, for 10-20 min followed by cooling at RT for 20 minutes.
2. The prediluted format is supplied in a dropper bottle and is optimized for use in IHC. After epitope retrieval step (if required) , drip mAb solution onto the tissue section and incubate at RT for 30 min.
Specificiy: Does not react with mouse and rat
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: N/A
Validation: N/A
Isoform: N/A
Purification: Protein G affinity chromatography
Clonality: Monoclonal
Clone: SPM336
Isotype: IgG1
Conjugate: Unconjugated
Physical State: Liquid
Buffer: PBS with 0.1 mg/ml BSA and 0.05% sodium azide
Concentration: 0.2 mg/mL
Storage Condition: Aliquot and Store at 2-8˚C. Avoid freez-thaw cycles.
Alternate Name: Bax Antibody: BCL2L4, BCL2L4, Apoptosis regulator BAX, Bcl-2-like protein 4, Bcl2-L-4
User Note: Optimal dilutions for each application to be determined by the researcher
BACKGROUND: Recognizes a protein of 21kDa, identified as the Bax protein. This mAb is highly specific to Bax and shows no cross-reaction with Bcl-2 or Bcl-X protein. Bcl-2 blocks cell death following a variety of stimuli. Bax has extensive amino acid homology with Bcl-2 and it homodimerizes and forms heterodimers with Bcl-2. Overexpression of Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3 dependent cell line, and Bax also counters the death repressor activity of Bcl-2.