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TANK binding kinase (TBK) is a serine/threonine kinase with a critical role in innate immune response and inflammation. This ubiquitously expressed enzyme has a range of substrates leading to additional roles in autophagy, cell proliferation and growth and insulin signaling.
TANK binding kinase (TBK) EC 18.104.22.168 is a ubiquitously expressed serine/threonine kinase belonging to the IκB Kinase (IKK) family, which regulates NF-κB signaling. This kinase has a range of substrates, leading to involvement in multiple pathways including immune response and inflammation, autophagy, cell proliferation and growth and insulin signaling.
TBK has a critical role in innate immunity and inflammation and functions downstream of multiple interferon (IFN) inducing pathways which are activated following pathogen sensing. When toll-like receptors are activated, TBK associates with TANK and TRAF3 to phosphorylate interferon regulatory factors (IRFs). This allows nuclear translocation of IRFs leading to transcriptional activation of antiviral and proinflammatory genes. Additionally, TBK can phosphorylate other transcription factors (STAT6), ubiquitin E3 ligases (Act1, PELI1, TRIM27) and other kinases including IKKα, IKKβ, Akt and mNIK.
TBK has the ability to autophosphorylate and so is highly regulated to avoid aberrant activation. This occurs through intracellular localization; TBK needs to be recruited to signaling complexes by adapter proteins. The physical structure of the TBK protein also limits autophosphorylation.
Certain mutations within the TBK gene are associated with neuroinflammatory and neurodegenerative disorders such as Amylotrophic Lateral Sclerosis (ALS), Frontotemporal Dementia (FTD), Normal Tension Glaucoma (NTG) and Childhood Herpes Encephalitis (HSE). In these conditions mutations in TBK lead to dysregulated autophagy.
Tocris offers the following scientific literature for TANK Binding Kinase to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.