IFITM1 Antibody #13126
Filter:
- WB
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 14 |
SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
IFITM1 Antibody recognizes endogenous levels of total IFITM1 protein. This antibody does not cross-react with IFITM2 or IFITM3 proteins.
Species Reactivity:
Human
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro20 of human IFITM1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Background
Interferon-induced transmembrane protein (IFITM) family members are composed of short amino- and carboxy-termini, two transmembrane domains, and a cytoplasmic domain (1). There are four family members in humans: IFITM1, IFITM2, IFITM3, and IFITM5 (2,3). Mice have two additional family members, IFITM6 and IFITM7 (2,3). Basal expression of IFITM proteins is observed in some cells and expression can also be induced by type I and type II interferons (4-6). The primary function of IFITM family proteins appears to be viral restriction, as IFITM proteins inhibit cytosolic entry of viruses by preventing fusion of viral and host membranes (7,8). The mechanism by which IFITM proteins inhibit fusion is unclear. Although IFITM proteins are present on both the plasma membrane and intracellular membranes, they most effectively restrict viral fusion in late endosomes and lysosomes (8,9). In addition, different family members exhibit specific viral preferences (9). For example, IFITM3 is most effective at restricting influenza A infection, while IFITM1 is more successful in controlling filoviruses and SARS (9,10).
- Diamond, M.S. and Farzan, M. (2013) Nat Rev Immunol 13, 46-57.
- Lange, U.C. et al. (2003) BMC Dev Biol 3, 1.
- Hickford, D. et al. (2012) BMC Genomics 13, 155.
- Reid, L.E. et al. (1989) Proc Natl Acad Sci U S A 86, 840-4.
- Lewin, A.R. et al. (1991) Eur J Biochem 199, 417-23.
- Friedman, R.L. et al. (1984) Cell 38, 745-55.
- Brass, A.L. et al. (2009) Cell 139, 1243-54.
- Feeley, E.M. et al. (2011) PLoS Pathog 7, e1002337.
- Huang, I.C. et al. (2011) PLoS Pathog 7, e1001258.
- Everitt, A.R. et al. (2012) Nature 484, 519-23.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意,否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件,除非书 CST 的合法授书代表以书面形式书独接受, 否书均被拒书,并且无效。
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For Research Use Only. Not For Use In Diagnostic Procedures.
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