research use only
Cat.No.: F7245
| Dilution |
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| Application |
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| WB, IP, IF |
| Reactivity |
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| Human, Mouse, Rat, Monkey |
| 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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| 27 kDa |
| Positive Control | 293 cells;HepG2 cells;C2C12 cells;KNRK cells;NBTII cells;HeLa cells |
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| Negative Control |
| Specificity |
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| eIF6 Antibody [A13F7] detects endogenous levels of total eIF6 protein. |
| Clone |
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| A13F7 |
| Synonym(s) |
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| Eukaryotic translation initiation factor 6; eIF-6; B(2)GCN homolog; B4 integrin interactor; CAB; p27(BBP); EIF6; EIF3A; ITGB4BP |
| Background |
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| eIF6 (eukaryotic initiation factor 6, also known as EIF6 or p27BBP1) is a highly conserved nucleolocytoplasmic protein that, despite lacking homology to canonical translation initiation factors, plays a fundamental dual role in ribosome biogenesis and translation control by binding the intersubunit face of free 60S ribosomal subunits. eIF6 adopts a flat, elongated shape with nine α-helices forming two domains that dock into the central protuberance and P-site of the 60S subunit, stabilized by key residues such as Arg133 and Lys151, and requires phosphorylation (notably at Ser174) for its regulated release. eIF6 acts as an anti-association factor, sequestering mature 60S subunits to prevent their premature joining with 40S subunits, thereby maintaining translational fidelity and quality control; in the nucleolus, it facilitates 60S maturation through interactions with SBDS and EFL1, which, via GTP hydrolysis, evict eIF6 and license subunits for translation, thus dynamically coupling ribosome recycling to protein synthesis rates. eIF6 integrates mTOR/S6K signaling to align ribosome availability with cellular growth demands, and associates with RISC to promote miRNA-mediated translational silencing or recycling blocks, its deletion abolishes miRNA repression. eIF6 dysregulation is implicated in Shwachman-Diamond syndrome (where SBDS mutations trap eIF6 and hinder 60S-40S joining), while its overexpression in various cancers (such as colorectal and gastric) drives unrestrained translation and cyclin D1 upregulation, contributing to tumorigenesis and metabolic imbalance. |
| References |
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