Human OAS2 (2'-5'-oligoadenylate synthase 2) ELISA Kit
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Product specifications
| Category | ELISA Kits |
| Reactivity | Human |
| Detection Method | Colorimetric |
| Assay Data | 4 hours |
| Assay Type | Sandwich ELISA, Double Antibody |
| Test Range | 0.313-20ng/ml |
| Sensitivity | 0.188ng/ml |
| Size 1 | 96T |
| Tested Applications | ELISA |
| Sample Type | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
| Availability | Shipped within 10-14 working days. |
| Storage | 2-8 °C for 12 months |
| UniProt ID | P29728 |
| Alias | 2'-5'-oligoadenylate synthase 2, (2-5')oligo(A) synthase 2, 2-5A synthase 2, p69 OAS / p71 OAS, p69OAS / p71OAS, OAS2 |
| Background | Elisa kits for OAS2 |
| Status | RUO |
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Human OAS2 (2'-5'-oligoadenylate synthase 2) ELISA Kit
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OAS2 antibody
Interferon-induced, dsRNA-activated antiviral enzyme which plays a critical role in cellular innate antiviral response. In addition, it may also play a role in other cellular processes such as apoptosis, cell growth, differentiation and gene regulation. Synthesizes higher oligomers of 2'-5'-oligoadenylates(2-5A) from ATP which then bind to the inactive monomeric form of ribonuclease L(RNase L) leading to its dimerization and subsequent activation. Activation of RNase L leads to degradation of cellular as well as viral RNA, resulting in the inhibition of protein synthesis, thus terminating viral replication. Can mediate the antiviral effect via the classical RNase L-dependent pathway or an alternative antiviral pathway independent of RNase L.
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Interferon-induced, dsRNA-activated antiviral enzyme which plays a critical role in cellular innate antiviral response. In addition, it may also play a role in other cellular processes such as apoptosis, cell growth, differentiation and gene regulation. Synthesizes higher oligomers of 2'-5'-oligoadenylates(2-5A) from ATP which then bind to the inactive monomeric form of ribonuclease L(RNase L) leading to its dimerization and subsequent activation. Activation of RNase L leads to degradation of cellular as well as viral RNA, resulting in the inhibition of protein synthesis, thus terminating viral replication. Can mediate the antiviral effect via the classical RNase L-dependent pathway or an alternative antiviral pathway independent of RNase L.
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