research use only

Phospho-4E-BP1 (Thr37/46) Antibody [E9G24]

Cat.No.: F0150

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:800 - 1:3200
    1:200 - 1:800
    1:50 - 1:200
    Application
    WB, IHC, IF, FCM
    Reactivity
    Human, Mouse, Rat, Monkey, D. melanogaster
    Source
    Rabbit Monoclonal Antibody
    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
    15 to 20 kDa
    Positive Control Human colon carcinoma; Human lymphoma; Human colon; 3T3 cells; Jurkat cells; LNCaP cells
    Negative Control LNCaP cells (LY294002-treated)

    Datasheet & SDS

    Biological Description

    Specificity
    Phospho-4E-BP1 (Thr37/46) Antibody [E9G24] detects endogenous levels of total 4E-BP1 protein only when it is phosphorylated at Thr37/46.
    Clone
    E9G24
    Synonym(s)
    Eukaryotic translation initiation factor 4E-binding protein 1; 4E-BP1; eIF4E-binding protein 1; Phosphorylated heat- and acid-stable protein regulated by insulin 1 (PHAS-I); EIF4EBP1
    Background
    Phospho-4E-BP1 (Thr37/46) refers to eukaryotic initiation factor 4E-binding protein 1 phosphorylated at priming sites Thr37/46 by mTORC1, a key translational repressor that intrinsically lacks stable secondary structure but adopts helical conformations upon Raptor binding via conserved YXXØΦ/RAIP motifs flanking the central TOS domain. Thr37/46 phosphorylation in flexible loops creates negative charge clusters that electrostatically complement Raptor's basic pocket (Arg770/Lys841), stabilizing mTORC1 docking and inducing disorder-to-helix transitions that prime hierarchical Ser65/Thr70 phosphorylation while maintaining eIF4E affinity. Unphosphorylated 4E-BP1 binds eIF4E's dorsal surface via Y37-ITDF motif, blocking eIF4G recruitment to m7GpppN caps and repressing cap-dependent translation of 5'TOP mRNAs (ribosomal proteins, translation factors); Thr37/46 phosphorylation initiates a cascade releasing 4E-BP1 from eIF4E, assembling eIF4F to stimulate global protein synthesis under nutrient/growth factor stimulation via PI3K/AKT/mTORC1. This switch fine-tunes metabolic/anabolic balance, with phospho-Thr37/46 marking early mTORC1 activation. Hyperphosphorylation drives oncogenesis in cancers via upregulated translation, while therapeutic hypophosphorylation (rapalogs/ATP-competitive mTORi) reactivates tumor suppression and ameliorates mTORopathies.
    References
    • https://pubmed.ncbi.nlm.nih.gov/10364159/
    • https://pubmed.ncbi.nlm.nih.gov/33852892/

    Tech Support

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3

    If you have any other enquiries, please leave a message.