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this study shows that STAT6 negatively regulates IFNphi1 production by attenuating the kinase activity of TANK-binding kinase 1
Fish IRF6 is distinguished from the homolog of mammals by being a positive regulator of IFN transcription and phosphorylated by MyD88 and TBK1, suggesting that differences in the IRF6 regulation pattern exist between lower and higher vertebrates.
Classical swine fever virus non-structural protein 4B binds TBK1.
TBK1 mutation p.Ile334Thr was identified as a pathogenic variant in frontotemporal dementia.
TANK-binding kinase 1 protein (TBK1) and IKK-epsilon protein (IKKepsilon) phosphorylate the kinase receptor (TNFRSF)-interacting serine-threonine kinase 1 (RIPK1) and prevent RIPK1-dependent cell death.
Installation of a tetrazole carboxylic acid bioisostere improved potency to 200 and 400 nM toward IKKepsilon and TBK1, respectively.
this study shows that TBK1 is a key regulator and potential treatment target for interferon positive Sjogren's syndrome, systemic lupus erythematosus and systemic sclerosis
The NLRP2-TBK1 axis may serve as an additional signaling cascade to maintain immune homeostasis in response to viral infection.
Activation of TANK-binding kinase 1 (TBK1) is inhibited by Zika virus NS5 protein. The interaction between ubiquitin-like domain of TBK1 and NS5 results in less complex of TBK1 and TNF (tumor necrosis factor) receptor-associated factor 6 (TRAF6), leading to dampened TBK1 activation and IRF3 phosphorylation.
these findings expand our knowledge on the molecular mechanism of ubiquitin- decorated autophagic substrates recognition by OPTN as well as the mutual regulation between OPTN and TBK1 in selective autophagy.
Study identified TTC4 as a TBK1 interactor and positive regulator of Sendai virus-induced innate immunity.
The study links the Arg573Gly TBK1 mutation with an autosomal dominant primary lateral sclerosis/dementia phenotype.
Of the whole cohort of patients with Motor Neuron Disease and Frontotemporal Dementia, 2 patients harboured a mutation in the TANK-binding kinase 1 (TBK1).
TBK1 is not only a recurrent cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but a cause of other neurodegenerative disorders like progressive cerebellar ataxia and cerebellar ataxia.
It contributes to the etiology of sporadic amyotrophic lateral sclerosis in Japanese patients.
TANK-binding kinase 1 (TBK1) loss-of-function (LoF) mutations are risk of Alzheimer's disease.
Cdc25A negatively regulates the antiviral immune response by inhibiting TBK1 activity.
Two-stage meta-analysis to investigate the frequency of TBK1 mutations in amyotrophic lateral sclerosis/frontotemporal dementia (ALS/FTD) patients and the association between the mutations and risk of ALS/FTD spectrum showed that TBK1 loss of function and missense mutations are not frequently found in ALS/FTD patients, and both of them are associated with an increased risk for ALS/FTD spectrum.
This study describes the crystal structures of optineurin/TBK1 complex and the related NAP1/TBK1 complex, uncovering the detailed molecular mechanism governing the optineurin and TBK1 interaction, and revealing a general binding mode between TBK1 and its associated adaptor proteins.
Low TBK1 expression is associated with RNA virus infections.
Loss of TBK1 by Us11 promotes HSV-1 infection through Formation of the Us11-Hsp90 Complex.
This study supports the implication of TBK1 in Amyotrophic Lateral Sclerosis and Cognitive Decline pathogenesis in Italy.
work identifies the TRIM23-TBK1-p62 axis as a key component of selective autophagy and further reveals a role for K27-linked ubiquitination in GTPase-dependent TBK1 activation
The genetic susceptibility induced by TBK1 heterozygosity can be compounded by aging-induced reduction of TAK1 expression in the brains to promote the activation of RIPK1 and amyotrophic lateral sclerosis and frontotemporal dementia
These data implicate a unique role for TBK1 in mediating bidirectional crosstalk between energy sensing and inflammatory signaling pathways in both over- and undernutrition.
In response to the presence of cytosolic DNA, STING translocates from the endoplasmic reticulum (ER) to the Golgi, and activates TANK-binding kinase 1 (TBK1), a cytosolic kinase that is essential for the activation of STING-dependent downstream signaling. TBK1 binds to STING at the Golgi, not at the ER.
Chronic innate immune activation of TBK1 suppresses mTORC1 activity, leading to dysregulated cellular metabolism.
IL-17 inhibits adipogenesis where a lack of IL-17 ameliorates glucose metabolism. As well, the inhibition of TBK1 reduces inflammation induced by IL-17. Therefore, IL-17 may be involved in the development of obesity and metabolic dysfunction in a TBK1-dependent manner.
Data show that TBK1 directly interacts with Exo84 through the coiled-coil domain of TBK1 and helical domain of Exo84, and knockdown of TBK1 blocked insulin-stimulated glucose uptake and GLUT4 translocation.
The TBK1 Y179A mutant failed to rescue type I IFN production by virally infected RAW264.7 macrophages deficient in TBK1
HERP Binds TBK1 To Activate Innate Immunity and Repress Virus Replication in Response to Endoplasmic Reticulum Stress
these studies reveal an additional regulatory function of TRIM8 in innate immune responses: TRIM8 catalyzes polyubiquitination of TRIF, resulting in disruption of TRIF-TBK1 interaction
TBK1 regulates p16 expression and retinal ganglion cell senescence.
functions in dendritic cells to regulate T cell homeostasis, autoimmunity, and antitumor immunity
USP38 inhibits type I interferon signaling by editing TBK1 ubiquitination through NLRP4 signalosome.
The authors report that Raf kinase inhibitory protein (RKIP) is essential for TBK1 activation and type I interferon production triggered by viral infection.
Upon stimulation with poly(I:C), malaria parasite-infected red blood cells (iRBCs), or vesicular stomatitis virus (VSV), FOSL1 "translocated" from the nucleus to the cytoplasm, where it inhibited the interactions between TNF receptor-associated factor 3 (TRAF3), TIR domain-containing adapter inducing IFN-beta (TRIF), and Tank-binding kinase 1 (TBK1) via impairing K63-linked polyubiquitination of TRAF3 and TRIF.
TBK1 complexes required for the phosphorylation of IRF3 and the production of interferon-beta have been identified.
this study reveals a previously unknown ICOS-TBK1 signaling pathway that specifies the commitment of germinal center follicular helper T cells
Innate immune responses to adenovirus vectors are largely TBK1-dependent in the spleen but TBK1-independent in the liver
Data show that the formation of a tripartite ribosomal protein S6 kinase 1 (S6K1)-STING membrane protein-TANK-binding kinase 1 (TBK1) complex was necessary for the activation of interferon regulatory factor-3 (IRF3).
This study suggest that TBK1 exerts pronociceptive effects in inflammatory nociception which are due to both modulation of NF-kappaB dependent genes and regulation of MAPKs and c-fos.
TRIM27 inhibits VSV infection-induced type I IFN production by promoting TBK1 degradation.
The NF-kappa-B (NFKB) complex of proteins is inhibited by I-kappa-B (IKB) proteins, which inactivate NFKB by trapping it in the cytoplasm. Phosphorylation of serine residues on the IKB proteins by IKB kinases marks them for destruction via the ubiquitination pathway, thereby allowing activation and nuclear translocation of the NFKB complex. The protein encoded by this gene is similar to IKB kinases and can mediate NFKB activation in response to certain growth factors.
serine/threonine-protein kinase TBK1
, TANK-binding kinase 1
, NF-kappa-B-activating kinase
, TANK binding kinase 1
, serine/threonine protein kinase TBK1
, serine/threonine-protein kinase TBK1-like
, NF-kB-activating kinase