Anti-Bax Rabbit Antibody [F1C6]

Catalog No.: F3518

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:200
    1:100 - 1:200
    1:100 - 1:400
    Application
    WB, IP, IF, FCM
    Reactivity
    Human
    Source
    Rabbit
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    20 kDa
    Positive Control MCF-7; A549; HepG2; ACHN; HT-1080
    Negative Control DU 145

    Datasheet & SDS

    Biological Description

    Specificity
    Bax (F1C6) Rabbit mAb detects endogenous levels of total Bax (F1C6) protein.
    Clone
    F1C6
    Synonym(s)
    Apoptosis regulator BAX, Bcl-2-like protein 4 (Bcl2-L-4), BAX, BCL2L4.
    Background
    Mitochondria play an essential role in cell survival by producing ATP through oxidative phosphorylation. The pro-apoptotic Bcl-2 family members Bax and Bak are pivotal regulators of programmed cell death. Normally existing as inert monomers, Bax and Bak can undergo activation to form oligomers that create pores in the mitochondrial outer membrane (MOM), triggering apoptosis. Their activity is tightly controlled by other Bcl-2 family proteins: BH3-only proteins directly activate Bax and Bak, while prosurvival Bcl-2 proteins inhibit them through direct binding. Bax, in particular, serves as a critical switch between cell life and death. Under resting conditions, Bax is mainly located in the cytosol in a monomeric, inactive state. Upon cellular stress, it undergoes a conformational change into an oligomeric form capable of permeabilizing the MOM. This structural transformation is a tightly regulated event, as inappropriate Bax activation poses a severe threat to cell viability. Bax balances stability and flexibility: the N- and C-terminal regions have auto-inhibitory features, with the α1–α2 loop covering a key activation site and the C-terminal α9 helix anchored within a regulatory groove. Activation triggers the release of these inhibitory elements. This permeabilization facilitates the release of apoptogenic molecules, including cytochrome c, which then activates caspase-9 and initiates the downstream caspase cascade, irrevocably committing the cell to apoptosis.
    References
    • https://pubmed.ncbi.nlm.nih.gov/24162660/
    • https://pubmed.ncbi.nlm.nih.gov/34389733/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
    If you have any other enquiries, please leave a message.

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