|Tested species reactivity||Human|
|Published species reactivity||Virus, Mouse|
|Host / Isotype||Mouse / IgG2a|
|Immunogen||Recombinant protein derived from the C-terminal region of the human IRF3 (interferon regulatory factor 3) protein|
|Storage buffer||PBS, pH 7.4|
|Contains||0.1% sodium azide|
|Tested Applications||Dilution *|
|ELISA (ELISA)||Assay Dependent|
|Immunofluorescence (IF)||Assay Dependent|
|Western Blot (WB)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
Interferons (IFN)s are involved in a multitude of immune interactions during viral infections and play a major role in both the induction and regulation of innate and adaptive antiviral mechanisms. During infection, host-virus interactions signal downstream molecules such as transcription factors such as IFN regulatory factor-3 (IRF3) which can act to stimulate transcription of IFN-alpha/beta genes. IRF3 is present in an inactive form in the cytoplasm of most cells. Following viral infection, IRF3 can be activated by Ikappa-B kinase-iota and TANK-binding kinase 1 (TBK1), whereupon IRF3 translocates to the nucleus. IRF3 can also be activated by stimulation of toll-like receptor 3 (TLR3) by dsRNA. IRF3 exists as at least two distinct isoforms.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Cyclic dinucleotides trigger ULK1 (ATG1) phosphorylation of STING to prevent sustained innate immune signaling.
39-2700 was used in immunocytochemistry and western blot to report that cyclic dinucleotides regulate the negative-feedback control of STING activity.
|Konno H,Konno K,Barber GN||Cell (155:688)||2013|
|Virus||Not Cited||Inhibition of Beta interferon induction by severe acute respiratory syndrome coronavirus suggests a two-step model for activation of interferon regulatory factor 3.||Spiegel M,Pichlmair A,Martínez-Sobrido L,Cros J,García-Sastre A,Haller O,Weber F||Journal of virology (79:2079)||2005|