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this study shows that STAT6 (zeige STAT6 Proteine) negatively regulates IFNphi1 production by attenuating the kinase activity of TANK-binding kinase 1
Fish IRF6 (zeige IRF6 Proteine) is distinguished from the homolog of mammals by being a positive regulator of IFN transcription and phosphorylated by MyD88 (zeige MYD88 Proteine) and TBK1, suggesting that differences in the IRF6 (zeige IRF6 Proteine) regulation pattern exist between lower and higher vertebrates.
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.
TANK-binding kinase 1 (TBK1) loss-of-function (LoF) mutations are risk of Alzheimer's disease.
Cdc25A (zeige CDC25A Proteine) 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 (zeige IGFALS Proteine)/FTD (zeige FTL Proteine)) patients and the association between the mutations and risk of ALS (zeige IGFALS Proteine)/FTD (zeige FTL Proteine) spectrum showed that TBK1 loss of function and missense mutations are not frequently found in ALS (zeige IGFALS Proteine)/FTD (zeige FTL Proteine) patients, and both of them are associated with an increased risk for ALS (zeige IGFALS Proteine)/FTD (zeige FTL Proteine) spectrum.
This study describes the crystal structures of optineurin (zeige OPTN Proteine)/TBK1 complex and the related NAP1 (zeige IL8 Proteine)/TBK1 complex, uncovering the detailed molecular mechanism governing the optineurin (zeige OPTN Proteine) 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 (zeige HSP90 Proteine) Complex.
This study supports the implication of TBK1 in Amyotrophic Lateral Sclerosis and Cognitive Decline pathogenesis in Italy.
work identifies the TRIM23 (zeige TRIM23 Proteine)-TBK1-p62 (zeige GTF2H1 Proteine) axis as a key component of selective autophagy and further reveals a role for K27 (zeige KRT27 Proteine)-linked ubiquitination in GTPase (zeige RACGAP1 Proteine)-dependent TBK1 activation
Given the critical roles of TBK1, important regulatory mechanisms are required to regulate its activity. Among these, Optineurin (Optn (zeige OPTN Proteine)) was shown to negatively regulate the interferon (zeige IFNA Proteine) response, in addition to its important role in membrane trafficking, protein secretion, autophagy and cell division.
Chronic innate immune activation of TBK1 suppresses mTORC1 activity, leading to dysregulated cellular metabolism.
IL-17 (zeige IL17A Proteine) inhibits adipogenesis where a lack of IL-17 (zeige IL17A Proteine) ameliorates glucose metabolism. As well, the inhibition of TBK1 reduces inflammation induced by IL-17 (zeige IL17A Proteine). Therefore, IL-17 (zeige IL17A Proteine) may be involved in the development of obesity and metabolic dysfunction in a TBK1-dependent manner.
Data show that TBK1 directly interacts with Exo84 (zeige EXO84 Proteine) through the coiled-coil domain of TBK1 and helical domain of Exo84 (zeige EXO84 Proteine), and knockdown of TBK1 blocked insulin (zeige INS Proteine)-stimulated glucose uptake and GLUT4 (zeige SLC2A4 Proteine) translocation.
The TBK1 Y179A mutant failed to rescue type I IFN production by virally infected RAW264.7 macrophages deficient in TBK1
HERP (zeige HERPUD1 Proteine) 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 (zeige TRIM8 Proteine) in innate immune responses: TRIM8 (zeige TRIM8 Proteine) catalyzes polyubiquitination of TRIF (zeige RNF138 Proteine), resulting in disruption of TRIF (zeige RNF138 Proteine)-TBK1 interaction
TBK1 regulates p16 expression and retinal ganglion cell senescence.
USP38 inhibits type I interferon signaling by editing TBK1 ubiquitination through NLRP4 signalosome.
The authors report that Raf kinase inhibitory protein (RKIP (zeige PEBP1 Proteine)) is essential for TBK1 activation and type I interferon (zeige IFNA Proteine) production triggered by viral infection.
Upon stimulation with poly(I:C), malaria parasite-infected red blood cells (iRBCs), or vesicular stomatitis virus (VSV), FOSL1 (zeige FOSL1 Proteine) "translocated" from the nucleus to the cytoplasm, where it inhibited the interactions between TNF receptor-associated factor 3 (TRAF3 (zeige TRAF3 Proteine)), TIR domain-containing adapter inducing IFN-beta (zeige IFNB1 Proteine) (TRIF (zeige RNF138 Proteine)), and Tank-binding kinase 1 (TBK1) via impairing K63-linked polyubiquitination of TRAF3 (zeige TRAF3 Proteine) and TRIF (zeige RNF138 Proteine).
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