research use only
Cat.No.: F0150
| Dilution |
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| Application |
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| WB, IHC, IF, FCM |
| Reactivity |
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| Human, Mouse, Rat, Monkey, D. melanogaster |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 15 to 20 kDa |
| Positive Control | Human colon carcinoma; Human lymphoma; Human colon; 3T3 cells; Jurkat cells; LNCaP cells |
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| Negative Control | LNCaP cells (LY294002-treated) |
| Specificity |
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| Phospho-4E-BP1 (Thr37/46) Antibody [E9G24] detects endogenous levels of total 4E-BP1 protein only when it is phosphorylated at Thr37/46. |
| Clone |
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| E9G24 |
| Synonym(s) |
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| 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 |
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| 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 |
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