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Biochem/physiol Actions

TBK1 (TANK-binding kinase 1) can phosphorylate numerous proteins, like optineurin, P62 (sequestosome 1) and interferon regulatory factor 3 (IRF3). It participates in various signaling pathways, namely, autophagy, antiviral and antibacterial innate immunity responses, oncogenic transformation and expression of inflammatory mediators. Mutations in this gene are linked with sporadic amyotrophic lateral sclerosis (SALS), familial ALS (FALS) and frontotemporal dementia. Defects in TBK1 suppresses autophagy, causing the accumulation of damaged mitochondria, thereby leading to neurodegeneration. Alteration in the copy number of TBK1 gene is associated with normal tension glaucoma. TBK1, also known as NAK or NFκB-activating kinase, is an upstream protein kinase that can phosphorylate and activate the IkB kinases. 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 NFκB 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.

General description

TBK1 (TANK-binding kinase 1) gene is located on human chromosome 12q14. It is a serine/threonine protein kinase. The encoded protein has a kinase domain, a ubiquitin-like domain, an α-helical scaffold dimerization domain and a small adaptor-binding motif.

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Physical form

Supplied in 50mM Tris-HCl, pH 7.5, 150mM NaCl, 10mM glutathione, 0.1mM EDTA, 0.25mM DTT, 0.1mM PMSF, 25% glycerol.

Preparation Note

after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles