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TBK1TANK Binding Kinase 1
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Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor cell survival.
(52) TRIF recruits another signalling complex involving the non-canonical IKKs, TBK1 and IKKi (IKKe), which catalyze the phosphorylation of IRF3 and induce nuclear translocation to mediate transcription of target genes.
To add the complexity, novel IKK-related kinases, IKKe (also known as IKK-i) and TBK1, have been implicated in obesity- and inflammation-induced insulin resistance [85, 86].
For examples, K27-linked polyubiquitination of STING provides a scaffold to recruit TBK1 and IRF3 [41]; iRhom2 can antagonize polyubiquitination of MAVS and STING and consequently maintain the stability of these proteins [42, 43].
Finch et al., "Whole-genome sequencing reveals important role for TBK1 and OPTN mutations in frontotemporal lobar degeneration without motor neuron disease," Acta Neuropathologica, vol.
MyD88-independent pathway involves TRIF and TRAM adaptor proteins, the activation of TRAF3, and downstream induction of TBK1 and IKK[epsilon], which are responsible for the recruitment and activation of the transcription factor, IFN regulatory factor 3 (IRF3).
This initiates the recruitment and activation of downstream proteins (TBK1 and IRF3) that induce the transcription and translation of type I interferon, a potent anti-viral cytokine.
The pivotal role of TBK1 in inflammatory responses mediated by macrophages.
Collins, "TBK1: a new player in ALS linking autophagy and neuroinflammation," Molecular Brain, vol.
A similar IRF7 negative regulatory mechanism was described by Liang and colleagues [46], in which they observed that ATF4, a stress response molecule induced by viral infection, is able to inhibit IRF7 activation by inhibiting the phosphorylation of Ser477/Ser479 by TBK1 and IKKe, thereby suppressing the gene expression of IFN-[alpha] and IFN-[beta].
Unsurprisingly, in contrast to PI3K signaling, the early TLR-dependent DC activation is mediated by downstream AKT signaling nodes, which phosphorylates and activates the rate-limiting enzyme hexokinase 2 (HK2) by a TANK-binding kinase 1 (TBK1) and inhibitor of nuclear factor-[kappa]B kinase subunit-[epsilon] (IKK [epsilon]) [53-55].
TBK1 and IKK[epsilon] are then free to phosphorylate IRF3, which is activated upon phosphorylation and dimerisation and stimulates the production of type I interferons [48, 56].