
Anti-4E-BP1 (N63) Antibody
Price on request
| SKU | Price | Quantity |
|---|---|---|
| A25402-100 | Price on request |
Description
This description has not been verified against the manufacturer's datasheet. Check the datasheet before you order, or ask us to confirm a specification. Ask us to confirm
Raised in rabbit against the N-terminal region of eukaryotic translation initiation factor 4E-binding protein 1, this unconjugated polyclonal reagent from Antibodies.com detects endogenous 4E-BP1 in human, mouse, and rat samples. The protein, also called PHAS-I, sits at a central node of mTORC1 signalling: in its hypophosphorylated state it sequesters the cap-binding factor eIF4E and blocks cap-dependent translation, whereas sequential phosphorylation at Thr37, Thr46, Ser65 and Thr70 releases eIF4E to drive protein synthesis, cell growth and proliferation.
Validated for western blot and immunohistochemistry, the antibody is supplied at 1 mg/ml in phosphate buffered saline (pH ~7.2) with 0.05% sodium azide as preservative, and the 100 µl vial is sufficient for routine use across multiple blotting membranes or tissue sections. For western blot, working concentrations in the 0.5–2 µg/ml range on 20–40 µg of total cell lysate resolve the characteristic 4E-BP1 banding pattern near 15–20 kDa, where mobility shifts between faster- and slower-migrating forms report on mTOR pathway activation. For IHC, 1–5 µg/ml on paraffin-embedded sections with overnight incubation at 4 °C gives clean cytoplasmic and nuclear staining in metabolically active tissues.
For storage, keep the vial refrigerated for short-term use (up to two weeks) or aliquot into single-use fractions and freeze at -20 °C for longer-term storage, since repeated freeze-thaw cycles reduce polyclonal titre. Because 4E-BP1 phosphorylation status is widely used as a direct readout of mTORC1 activity, this antibody is applied across cancer cell signalling, metabolic disease, neural plasticity and autophagy research, as well as in studies of insulin signalling and T-cell activation where cap-dependent translation is a key regulatory step.
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