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HOME > Product search results > Code No. M010-3 Anti-BAX (Human) mAb

Code No. M010-3

Anti-BAX (Human) mAb

Price

¥48,000

Availability (in Japan)

10 or more

(In Japan at 17:00,
Aug 6, 2020 in JST)

Size

100 µg

Data
  • Western Blotting

  • Immunoprecipitation

  • Flow Cytometry

  • Immunocytochemistry

  • Immunohistochemistry

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.)  
Immunogen (Antigen) Recombinant Human BAX protein
Reactivity [Gene ID]

Human[581], Mouse(-)

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
Citations

Western Blotting

  1. Wang Y et al. Deletion of INMAP postpones mitotic exit and induces apoptosis by disabling the formation of mitotic spindle. Biochem Biophys Res Commun. 518, 19-25 (2019)(PMID:31405563)
Product category
Research area
Apoptosis
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  • The availability is based on the information in Japan at 17:00, Aug 6, 2020 in JST.
  • The special price is shown in red color.
  • Please note that products cannot be ordered from this website. To purchase the items listed in this website, please contact us or local distributers.
  • Abbreviations for applications:
    WB: Western Blotting, IH: Immunohistochemistry, IC: Immunocytochemistry, IP: Immunoprecipitation
    FCM: Flow Cytometry, NT: Neutralization, IF: Immunofluorescence, RIP: RNP Immunoprecipitation
    ChIP: Chromatin Immunoprecipitation, CoIP: Co-Immunoprecipitation
    DB: Dot Blotting, NB: Northern Blotting, RNA FISH: RNA Fluorescence in situ hybridization
  • For applications and reactivity:
    *: The use is reported in a research article (Not tested by MBL). Please check the data sheet for detailed information.
    **: The use is reported from the licenser (Under evaluation or not tested by MBL).
  • For storage temparature: RT: room temparature
  • Please note that products in this website might be changed or discontinued without notification in advance for quality improvement.