TANK Binding Kinase

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.

Products

Background

Literature (2)

Pathways (2)

TANK Binding Kinase Inhibitors
Cat. No.	Product Name / Activity
4857	Amlexanox
	Selective inhibitor of TBK
4318	BX 795
	Inhibits TBK; Also inhibits PDPK1, Aurora B and IKKε
5134	MRT 67307 dihydrochloride
	Potent inhibitor of TBK; also inhibits SIK, ULK1, ULK2, MARK1-4, IKKε and NUAK
5067	MRT 68601 hydrochloride
	Potent TBK inhibitor
Degraders
Cat. No.	Product Name / Activity
7259	TBK1 PROTAC^® 3i
	Potent TANK-binding kinase 1 (TBK1) Degrader
Controls
Cat. No.	Product Name / Activity
7260	TBK1 control PROTAC^® 4
	Negative control for TBK1 PROTAC^® 3i (Cat. No. 7259)

TANK binding kinase (TBK) EC 2.7.11.1 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.

External sources of pharmacological information for TANK Binding Kinase :

IUPHAR Receptor Code

BJP Guide

Literature for TANK Binding Kinase

Tocris offers the following scientific literature for TANK Binding Kinase to showcase our products. We invite you to request* your copy today!

*Please note that Tocris will only send literature to established scientific business / institute addresses.

Autophagy Scientific Review

Written by Patricia Boya and Patrice Codogno, this review summarizes the molecular mechanisms, physiology and pathology of autophagy. The role of autophagy in cell death and its links to disease are also discussed. Compounds available from Tocris are listed.

Autophagy Poster

Autophagy is a cellular process used by cells for degradation and recycling. Written by Patricia Boya and Patrice Codogno, this poster summarizes the molecular machinery, physiology and pathology of autophagy. Compounds available from Tocris are listed.

Pathways for TANK Binding Kinase

NF-κB Signaling Pathway

NF-κB signaling plays an important role in inflammation, the innate and adaptive immune response and stress. Dysregulated signaling can occur in inflammatory and autoimmune diseases.

Toll-like Receptor Signaling Pathway

TLR signaling is involved in the cellular response to threatening molecules such as bacteria and viruses. It results in an inflammatory and immmunological response.

TANK Binding Kinase