Code No. | M010-3 | |
Anti-BAX (Human) mAb | ||
Price | ¥52,800 | |
Size | 100 µg | |
Availability (in Japan) | 10 or more
(In Japan at 17:33, Apr 26, 2024 in JST) |
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Clonality | Monoclonal | |
Clone | 4F11 | |
Isotype (Immunized Animal) |
Mouse IgG2bκ | |
Applications | WB 0.1-1 µg/mL IP 5-10 µg /200 µL of cell extract from 5x106 cells FCM 5-10 µg/mL (final concentration) IC 10 µg/mL IH 10 µg/mL (Heat treatment is necessary for paraffin embedded sections.) |
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Immunogen (Antigen) |
Recombinant Human BAX protein | |
Reactivity [Gene ID] | Human[581], Mouse(-) |
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Storage buffer | lyophilized form. After reconstitution with 100 µL of distilled water, the IgG concentration should be 1mg/mL in PBS/1% sucrose, pH 7.2 | |
Storage temp. | 4°C | |
Conjugate | Unlabeled | |
Manufacturer | MBL | |
Alternative names | BCL2 associated X, apoptosis regulator | |
Background | Bax (Bcl-associated X protein) is a 21 kDa tumor suppressor protein that suppresses tumorigenesis and stimulates apoptosis in vivo. Bax has extensive amino acid homology to Bcl-2. It can homodimerize through its BH3 domain and it forms heterodimers with other Bcl-2 family members through its BH1 and BH2 domains. Overexpression of Bax promotes apoptosis and counters the death repressor activity of Bcl-2 and Bcl-xL. It is believed that the ratio of Bcl-2/Bax complexes to free protein controls the relative susceptibility of cells to death stimuli. Apoptotic stimuli cause the translocation of monomeric Bax from the cytosol to the mitochondria where it forms Bax homodimers. Localization of Bax to the mitochondria results in the activation of caspase-3, membrane blebbing, and nuclear fragmentation. Bax also induces mitochondrial dysfunction by increasing mitochondrial membrane permeability. It accelerates the opening of the mitochondrial porin channel VDAC, thus regulating the release of cytochrome c during apoptosis. | |
Related products | M160-3 Anti-UVRAG mAb |
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Product category | Research area:Apoptosis | |
Data | ||
Citations | Western Blotting
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