OAS1 (D1W3A) Rabbit mAb #14498
- WB
- IP
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 40, 44 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:10 - 1:50 |
| Immunoprecipitation | 1:50 |
Storage
Protocol
Specificity / Sensitivity
OAS1 (D1W3A) Rabbit mAb recognizes endogenous levels of total OAS1 protein. This antibody cross-reacts with an unidentified protein of 100 kDa in some cell lines.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp90 of human OAS1 protien.
Background
2’-5’-oligoadenylate synthetase 1 (OAS1) is an antiviral protein induced by type 1 interferon that plays a key role in the cellular innate immune response (1). The OAS family of proteins includes OAS1, OAS2, OAS3, and OASL in humans (2). The OAS1 enzyme produces the second messenger 2’-5’-linked oligoadenylate in response to cytosolic dsRNA. These 2’-5’-linked oligoadenylates bind to the ribonuclease RNase L, which then degrades viral and cellular RNA (3). Research studies indicate that the OAS1 system inhibits protein synthesis and induces apoptosis in virally infected cells, which limits viral infection (4). Alternative splicing generates multiple isoforms of human OAS1, including p41 and the canonical p46 (5,6). Polymorphisms in the corresponding OAS1 gene have been examined for possible association with increased susceptibility to type 1 diabetes mellitus, multiple sclerosis, and infection by viral pathogens (7,8).
- Schoggins, J.W. et al. (2011) Nature 472, 481-5.
- Chebath, J. et al. (1987) Nature 330, 587-8.
- Dong, B. and Silverman, R.H. (1997) J Biol Chem 272, 22236-42.
- Castelli, J.C. et al. (1998) Cell Death Differ 5, 313-20.
- Benech, P. et al. (1985) EMBO J 4, 2249-56.
- Saunders, M.E. et al. (1985) EMBO J 4, 1761-8.
- Cagliani, R. et al. (2012) Hum Genet 131, 87-97.
- Tessier, M.C. et al. (2006) J Med Genet 43, 129-32.
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