Human Interferon-induced Protein with Tetratricopeptide Repeats 2, IFIT2 ELISA Kit
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IFN-induced antiviral protein which inhibits expression of viral messenger RNAs lacking 2'-O-methylation of the 5' cap. The ribose 2'-O-methylation would provide a molecular signature to distinguish between self and non-self mRNAs by the host during viral infection. Viruses evolved several ways to evade this restriction system such as encoding their own 2'-O-methylase for their mRNAs or by stealing host cap containing the 2'-O-methylation (cap snatching mechanism). Binds AU-rich viral RNAs, with or without 5' triphosphorylation, RNA-binding is required for antiviral activity. Can promote apoptosis.
Fully tested in-house by ABMIUM, or supported by an advanced validation report from a partner reviewed by ABMIUM. Highest confidence. Non-conformities fully supported under the ABMIUM Product Promise.
Quality verified. Independent collaborator or expected-performance data available. Product meets ABMIUM quality standards.
Expected to work based on structural and biochemical data. Not yet directly tested by ABMIUM or a collaborator. No non-conformity support for this combination.
Not recommended for this application or species/sample combination. This may indicate either evidence of unsuitability or that the combination has not been tested and therefore cannot currently be recommended.
Evidence status by application and model.
| Evidence | Serum | Plasma | Cell culture supernatants | Ascites | Tissue homogenates |
|---|---|---|---|---|---|
| Compatibility |
This product is manufactured by BT LAB and sold through ABMIUM without relabelling.
ABMIUM supports global orders. Availability, shipping requirements and applicable import arrangements are confirmed before fulfilment where required.
Yes. Send your target, sample, application and experimental conditions through ABMIUM MATCH or technical support.
Unless the listing expressly states otherwise, ABMIUM products are supplied for research use only and are not for diagnostic or therapeutic use.