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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.
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
Given the critical roles of TBK1, important regulatory mechanisms are required to regulate its activity. Among these, Optineurin (Optn) was shown to negatively regulate the interferon response, in addition to its important role in membrane trafficking, protein secretion, autophagy and cell division.
we detected no statistical difference in age at diagnosis or maximum IOP when we compared patients with a TBK1 gene duplication and patients with a TBK1 gene triplication.
Human T-lymphotropic virus 1 Tax protein impairs K63-linked ubiquitination of STING and disrupted the interactions between STING and TBK1 to evade host innate immunity.
we investigated a large European study population of 2,538 European FTD-ALS spectrum patients to get a deeper appreciation of the mutation frequency, mutation spectrum, and the genotype-phenotype profile of TBK1 patient carriers.
These results outline a novel mechanism for the control of TBK1 activity and suggest USP1-UAF1 complex as a potential target for the prevention of viral diseases.
TRIM9s undergoes Lys-63-linked auto-polyubiquitination and serves as a platform to bridge GSK3beta to TBK1, leading to the activation of IRF3 signaling.
YPEL5 silencing enhanced the induction of IFNB1 by pattern recognition receptors and phosphorylation of TBK1/IKBKE kinases, whereas co-immunoprecipitation experiments revealed that YPEL5 interacted physically with IKBKE.
ZIKV infection of neuroepithelial stem cells and radial glial cells causes centrosomal depletion and mitochondrial sequestration of phospho-TBK1 during mitosis.
We report a five-generation pedigree with a complex pattern of primary open angle glaucoma(POAG) inheritance; familial clustering of POAG in this pedigree is consistent with dominant inheritance of a glaucoma-causing gene, mutations were not detected in genes previously associated with autosomal dominant glaucoma, suggesting the involvement of a novel disease-causing gene in this pedigree.
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.
Suggest that by reducing production of cAMP in adipocytes, PDE3B, IKKepsilon and TBK1 may contribute to the repression of energy expenditure during obesity.
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