The kinase TAK1 can activate the NIK-IκB as well as the MAP kinase cascade in the IL-1 signalling pathway

@article{NinomiyaTsuji1999TheKT,
  title={The kinase TAK1 can activate the NIK-I$\kappa$B as well as the MAP kinase cascade in the IL-1 signalling pathway},
  author={Jun Ninomiya-Tsuji and Kazuya Kishimoto and Atsushi Hiyama and Jun-ichiro Inoue and Zhaodan Cao and Kunihiro Matsumoto},
  journal={Nature},
  year={1999},
  volume={398},
  pages={252-256}
}
Interleukin-1 (IL-1) is a proinflammatory cytokine that has several effects in the inflammation process. When it binds to its cell-surface receptor, IL-1 initiates a signalling cascade that leads to activation of the transcription factor NF-κB and is relayed through the protein TRAF6 and a succession of kinase enzymes, including NF-κB-inducing kinase (NIK) and IκB kinases (IKKs). However, the molecular mechanism by which NIK is activated is not understood. Here we show that the MAPKK kinase… 
Interleukin-1 (IL-1) Receptor-Associated Kinase Leads to Activation of TAK1 by Inducing TAB2 Translocation in the IL-1 Signaling Pathway
TLDR
It is suggested that IRAK regulates the redistribution of TAB2 upon IL-1 stimulation and facilitates the formation of a TRAF6-TAB2-TAK1 complex, which is an essential step in the activation of TAK1 in theIL-1 signaling pathway.
ASK1 Inhibits Interleukin-1-induced NF-κB Activity through Disruption of TRAF6-TAK1 Interaction*
TLDR
It appears that the inhibition of NF-κB by ASK1 may result at least in part from the disruption of the TRAF6·TAK1 complex formation in the IL-1 signaling pathway.
Constitutive Association of TGF-β–Activated Kinase 1 with the IκB Kinase Complex in the Nucleus and Cytoplasm of Human Neutrophils and Its Impact on Downstream Processes
TLDR
The central role of TAK1 is established in controlling nuclear and cytoplasmic signaling cascades in primary neutrophils, making it a promising target for therapeutic intervention in view of the foremost role of neutrophil in several chronic inflammatory conditions.
THE ROLE OF KINASE ACTIVITY OF IRAK4 IN TLR/IL-1R-MEDIATED SIGNALING
TLDR
Inactivation of the IRAK4 kinase activity did not affect the levels of TLR/IL-1R-mediated NFκB activation, but a reduction of LPS-, R848and IL-1-mediated mRNA stability contributed to the reduced inactivation.
A20 INHIBITS NF-κB ACTIVATION DOWNSTREAM OF MULTIPLE MAP3 KINASES AND INTERACTS WITH THE IκB SIGNALOSOME
TLDR
Results suggest that the molecular target of A20 is more distal to the receptor than TRAFs as previously proposed, and the observation that A20 associates with IKKα and is phosphorylated upon IKKβ co-expression may suggest that A 20 interferes with some aspects of signalosome function.
The MAPK Kinase Kinase TAK1 Plays a Central Role in Coupling the Interleukin-1 Receptor to Both Transcriptional and RNA-targeted Mechanisms of Gene Regulation*
TLDR
Data indicate that the previously described three-pathway model of IL-8 induction is operative in response to a physiological stimulus, IL-1, and that the MAPKKK TAK1 couples theIL-1 receptor to both transcriptional and RNA-targeted mechanisms mediated by the three pathways.
The essential role of MEKK3 in TNF-induced NF-κB activation
TLDR
It is found that MEKK3 plays a critical role in TNF-induced NF-κB activation and functions downstream of receptor-interacting protein (RIP) and TNF receptor– associated factor 2.
Inhibition of Interleukin-1β-induced NF-κB Activation by Calcium/Calmodulin-dependent Protein Kinase Kinase Occurs through Akt Activation Associated with Interleukin-1 Receptor-associated Kinase Phosphorylation and Uncoupling of MyD88*
TLDR
It is suggested that CaMKK-dependent Akt activation inhibits IL-1β-induced NF-κB activation through interference with the coupling of IRAK1 to MyD88 and point mutation of this site abrogates the inhibitory effect of Akt on IRAK 1-mediated NF-kkB activation.
TAK1-dependent activation of AP-1 and c-Jun N-terminal kinase by receptor activator of NF-kappaB.
TLDR
Findings indicate that TAK1 is involved in the MAPK cascade and NF-kappaB pathway that is activated by RANK.
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TLDR
Overexpression of a catalytically inactive form of IKK-β blocked cytokine-induced NF-κB activation and suggested that an active IκB kinase complex may require three distinct protein kinases.
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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