NF-κB activation by tumour necrosis factor requires the Akt serine–threonine kinase

@article{Ozes1999NFBAB,
  title={NF-$\kappa$B activation by tumour necrosis factor requires the Akt serine–threonine kinase},
  author={Osman Nidai Ozes and Lindsey D. Mayo and Jason A. Gustin and Suzanne R. Pfeffer and Lawrence M. Pfeffer and David B Donner},
  journal={Nature},
  year={1999},
  volume={401},
  pages={82-85}
}
Activation of the nuclear transcription factor NF-κB by inflammatory cytokines requires the successive action of NF-κB-inducing kinase (NIK) and an IκB-kinase (IKK) complex composed of IKKα and IKKβ. Here we show that the Akt serine–threonine kinase is involved in the activation of NF-κB by tumour necrosis factor (TNF). TNF activates phosphatidylinositol-3-OH kinase (PI(3)K) and its downstream target Akt (protein kinase B). Wortmannin (a PI(3)K inhibitor), dominant-negative PI(3)K or kinase… 
Akt Is a Downstream Target of NF-κB*
The ubiquitously expressed transcription factor NF-κB and the serine-threonine kinase Akt both are involved in the promotion of cell survival. Although initially believed to operate as components of
Phosphatidylinositol 3-Kinase as a Mediator of TNF-Induced NF-κB Activation1
TLDR
The results indicate that a PI 3-kinase-regulated step in TNF-signaling is critical for the expression of NF-κB-dependent genes.
The PTEN Tumor Suppressor Protein Inhibits Tumor Necrosis Factor-induced Nuclear Factor κB Activity*
TLDR
PTEN, a tumor suppressor that inhibits PI 3-kinase function, impairs TNF activation of Akt and the IKK complex in 293 cells, and Expression of PTEN in PC-3 cells to a level comparable with that endogenously present in DU145 cells inhibited TNFactivation of NF-κB.
Interferon α/β Promotes Cell Survival by Activating Nuclear Factor κB through Phosphatidylinositol 3-Kinase and Akt*
Interferons (IFNs) play critical roles in host defense by modulating gene expression via activation of signal transducer and activator of transcription (STAT) factors. IFN-α/β also activates another
Akt Suppresses Apoptosis by Stimulating the Transactivation Potential of the RelA/p65 Subunit of NF-κB
TLDR
This work demonstrates that, unlike activated Ras, which can stimulate parallel pathways to activate both DNA binding and the transcriptional activity of NF-κB, Akt stimulates NF-kkB predominantly by upregulating of the transactivation potential of p65.
3-Phosphoinositide-dependent Protein Kinase-1-mediated IκB Kinase β (IKKB) Phosphorylation Activates NF-κB Signaling*
The IκB kinase (IKK)/NF-κB and phosphatidylinositol 3-OH-kinase/3-phosphoinositide-dependent protein kinase-1 (PDK1)/Akt pathways regulate various cellular functions, especially cell survival. These
PTEN Blocks Tumor Necrosis Factor-induced NF-κB-dependent Transcription by Inhibiting the Transactivation Potential of the p65 Subunit*
TLDR
It is found that the reintroduction of PTEN into prostate cells inhibited TNF-stimulated NF-κB transcriptional activity, and the transactivation potential of p65 following TNF stimulation could be rescued from PTEN-dependent repression by re-introducing expression constructs encoding activated forms of phosphoinositide 3-kinase, Akt, or Akt and IKK.
Raf Kinase Inhibitor Protein Interacts with NF-κB-Inducing Kinase and TAK1 and Inhibits NF-κB Activation
TLDR
It is shown here that RKIP also antagonizes the signal transduction pathways that mediate the activation of the transcription factor nuclear factor kappa B (NF-κB) in response to stimulation with tumor necrosis factor alpha (TNF-α) or interleukin 1 beta.
Stimulation of NFκB Activity by Multiple Signaling Pathways Requires PAK1*
The p21-activated kinase (PAK1) is a serine-threonine protein kinase that is activated by binding to the Rho family small G proteins Rac and Cdc42hs. Both Rac and Cdc42hs have been shown to regulate
Essential Role of Nuclear Factor (NF)-κB–Inducing Kinase and Inhibitor of κb (Iκb) Kinase α in Nf-κb Activation through Lymphotoxin β Receptor, but Not through Tumor Necrosis Factor Receptor I
TLDR
It is demonstrated that both NIK and IKKα are essential for the induction of NF-κB through LTβR, whereas the NIK–IKKα pathway is dispensable in TNFR-I signaling.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 20 REFERENCES
NF-κB-inducing kinase activates IKK-α by phosphorylation of Ser-176
Activation of the transcription factor NF-κB by inflammatory cytokines involves the successive action of NF-κB-inducing kinase (NIK) and two IκB kinases, IKK-α and IKK-β. Here we show that NIK
IκB Kinase-β: NF-κB Activation and Complex Formation with IκB Kinase-α and NIK
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.
Positive and Negative Regulation of IκB Kinase Activity Through IKKβ Subunit Phosphorylation
TLDR
IKKβ, not IKKα, is the target for proinflammatory stimuli, and once activated, IKKβ autophosphorylated at a carboxyl-terminal serine cluster, decreased IKK activity and may prevent prolonged activation of the inflammatory response.
IKK-1 and IKK-2: Cytokine-Activated IκB Kinases Essential for NF-κB Activation
Activation of the transcription factor nuclear factor kappa B (NF-κB) is controlled by sequential phosphorylation, ubiquitination, and degradation of its inhibitory subunit IκB. A large multiprotein
Identification and Characterization of an IκB Kinase
TLDR
CHUK is a NIK-activated IκB-α kinase that links TNF- and IL-1-induced kinase cascades to NF-κB activation and is greatly enhanced by NIK costimulation.
MAP3K-related kinase involved in NF-KB induction by TNF, CD95 and IL-1
TLDR
The findings indicate that NIK participates in an NF-KB-inducing signalling cascade common to receptors of the TNF/NGF family and to the interleukin-1 type-I receptor.
A cytokine-responsive IκB kinase that activates the transcription factor NF-κB
TLDR
IKK turns out to be the long-sought-after protein kinase that mediates the critical regulatory step in NF-κB activation, and phosphorylates IκBs on the sites that trigger their degradation.
Severe Liver Degeneration in Mice Lacking the IκB Kinase 2 Gene
TLDR
Results show that IKK2 is essential for mouse development and cannot be substituted with IKK1, another component of the IKK complex.
Embryonic Lethality, Liver Degeneration, and Impaired NF-κB Activation in IKK-β-Deficient Mice
TLDR
It is indicated that IKK-beta is crucial for liver development and regulation of NF-kappaB activity and that Ikk-alpha can only partially compensate for the loss of IKK, while basal and cytokine-inducible kinase activities of the IKK complex are greatly reduced.
TRADD–TRAF2 and TRADD–FADD Interactions Define Two Distinct TNF Receptor 1 Signal Transduction Pathways
TLDR
It is shown that TRADD directly interacts with TRAF2 and FADD, signal transducers that activate NF-kappa B and induce apoptosis, respectively, and these two TNFR1-TRADD signaling cascades appear to bifurcate at TRADD.
...
1
2
...