TBK1, also known as NAK or NFkB-activating kinase, is an upstream protein kinase that can phosphorylate and activate the IkB kinases (1). Activation of IkB kinases allows the phosphorylation of IkB protein which is then degraded via the ubiquitination pathway. This mechanism allows the activation of the NFkB transcriptional complex. TBK1 is a specific upstream regulator of IkB kinases and can also interact and the IkB protein TANK. TBK1 is a component of the virus-activated kinase that phosphorylate IRF3 and IRF7 allowing their dimerization and translocation to the nucleus, where they induce transcription of interferon (2).
NAK, T2K, FLJ11330
1. Tojima, Y. et al: NAK is an I-kappa-B kinase-activating kinase. Nature 404: 778-782, 2000.
2. Sharma, S. et al: Triggering the interferon antiviral response through an IKK-related pathway. Science 300: 1148-1151, 2003.
Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping:
Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Antonia RJ et al., TBK1 Limits mTORC1 by Promoting Phosphorylation of Raptor Ser877. Scientific reports September 2019 10.1038/s41598-019-49707-8
Hong Park Sun et al., IRAK4 as a Molecular Target in the Amelioration of Innate Immunity?Related Endotoxic Shock and Acute Liver Injury by Chlorogenic Acid Journal of Immunology November 2014 10.4049/jimmunol.1402101
Young Leea Jin et al., Celastrol blocks binding of lipopolysaccharides to a Toll-like receptor4/myeloid differentiation factor2 complex in a thiol-dependent manner Journal of Ethnopharmacology August 2015 10.1016/j.jep.2015.06.028
Young Lee Jin et al., Gambogic Acid Disrupts Toll-like Receptor4 Activation by Blocking Lipopolysaccharides Binding to Myeloid Differentiation Factor 2 Toxicological Research March 2015 10.5487/TR.2015.31.1.011
Inflammation, NfkB Pathway, Ser/Thr Kinases