Glycogen Synthase Kinase-3β Modulates Notch Signaling and Stability

@article{Foltz2002GlycogenSK,
  title={Glycogen Synthase Kinase-3$\beta$ Modulates Notch Signaling and Stability},
  author={Daniel R. Foltz and Michelle C. Santiago and Bridget E. Berechid and Jeffrey S. Nye},
  journal={Current Biology},
  year={2002},
  volume={12},
  pages={1006-1011}
}

Figures from this paper

Phosphorylation by Glycogen Synthase Kinase-3β Down-regulates Notch Activity, a Link for Notch and Wnt Pathways*
TLDR
The results suggest that cross-talk between Notch and Wnt pathways may be partially mediated by specific regulation of GSK-3β-dependent Notch phosphorylation, which has been shown previously to be crucial in regulating cytokine-specific cell differentiation.
Integrin-Linked Kinase Controls Notch1 Signaling by Down-Regulation of Protein Stability through Fbw7 Ubiquitin Ligase
TLDR
The results suggest that ILK down-regulated the protein stability of Notch1-IC through the ubiquitin-proteasome pathway by means of Fbw7.
AKT, NOTCH and GSK3β interact to trigger early myogenesis in vertebrate embryos
TLDR
Data support the hypothesis that transcription-independent function of NICD is a central mechanism driving myogenesis in early somites and suggests that, in this tissue, AKT, NOTCH and GSK3β interact in the cytoplasm to trigger a signaling cascade that leads to the formation of the early myotome in vertebrates.
GSK3β Interacts With CRMP2 and Notch1 and Controls T-Cell Motility
TLDR
It is concluded that GSK3β controls T- cell motility through interactions with CRMP2 and Notch1, which has important implications in adaptive immunity, T-cell mediated diseases and LFA-1-targeted therapies.
Role of STRAP in regulating GSK3β function and Notch3 stabilization
TLDR
A potential mechanism by which STRAP regulates GSK3β function and Notch3 stabilization is provided and this binding is enhanced in a proteasomal inhibition-dependent manner.
Regulation of Notch1/NICD and Hes1 expressions by GSK-3α/β
TLDR
Results indicate that GSK-3α is a negative regulator of Notch1/NICD, and at least three Thr residues in Notch 1 are critical for its response to LiCl, which increased not only the transcriptional activity of endogenous NICD but also Hes1 mRNA levels.
Glycogen Synthase Kinase-3β Regulates NF-κB1/p105 Stability*
TLDR
Interestingly, the increased sensitiveness to TNF-α-induced death occurring in GSK-3β–/– fibroblasts, which is coupled to a perturbation of p50/105 ratio, can be reproduced by p105 silencing in wild-type fibro Blasts.
GSK-3: Functional Insights from Cell Biology and Animal Models
TLDR
The various animal models that have been employed to dissect the functions of GSK-3 in brain development and function through the use of conventional or conditional knockout mice as well as transgenic mice reveal fundamental roles for these protein kinases in memory, behavior, and neuronal fate determination and provide insights into possible therapeutic interventions.
Glycogen synthase kinase-3 beta (GSK3β)-mediated phosphorylation of ETS1 promotes progression of ovarian carcinoma
TLDR
It is shown that ETS1 forms a complex with glycogen synthase kinase-3β (GSK3β) and that the GSK3β/ETS1/MMP-9 axis may regulate the biological aggressiveness of ovarian cancer and can serve as a prognostic factor in patients with this malignancy.
Serum- and glucocorticoid-inducible kinase 1 (SGK1) controls Notch1 signaling by downregulation of protein stability through Fbw7 ubiquitin ligase
TLDR
It is reported that the serum- and glucocorticoid-inducible protein kinase SGK1 remarkably reduced the protein stability of the active form of Notch1 through Fbw7.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 59 REFERENCES
Drosophila shaggy kinase and rat glycogen synthase kinase-3 have conserved activities and act downstream of Notch
TLDR
It is reported here that, in transgenic flies, GSK-3/β can substitute for shaggy, and the results indicate thatShaggy/GSK-3 is part of a signalling pathway downstream of Notch, which is related to signal transduction pathways in vertebrates.
SEL-10 Is an Inhibitor of Notch Signaling That Targets Notch for Ubiquitin-Mediated Protein Degradation
TLDR
It is shown here that the F-box/WD40 repeat protein SEL-10 negatively regulates Notch receptor activity by targeting the intracellular domain of Notch receptors for ubiquitin-mediated protein degradation.
Phosphorylation of Axin, a Wnt Signal Negative Regulator, by Glycogen Synthase Kinase-3β Regulates Its Stability*
TLDR
The results suggest that the phosphorylation of Axin is important for the regulation of its stability and that Wnt down-regulates Axin through Dvl.
Requirement for glycogen synthase kinase-3β in cell survival and NF-κB activation
TLDR
It is shown that disruption of the murine GSK-3β gene results in embryonic lethality caused by severe liver degeneration during mid-gestation, a phenotype consistent with excessive tumour necrosis factor (TNF) toxicity, as observed in mice lacking genes involved in the activation of the transcription factor activation NF-κB.
Requirement for glycogen synthase kinase-3beta in cell survival and NF-kappaB activation.
TLDR
It is shown that disruption of the murine GSK-3beta gene results in embryonic lethality caused by severe liver degeneration during mid-gestation, a phenotype consistent with excessive tumour necrosis factor (TNF) toxicity, as observed in mice lacking genes involved in the activation of the transcription factor activation NF-kappaB.
A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain
TLDR
It is reported that, in mammalian cells, PS1 deficiency also reduces the proteolytic release of NICD from a truncated Notch construct, thus identifying the specific biochemical step of the Notch signalling pathway that is affected by PS1.
Functional Interaction between SEL-10 , an F-box Protein , and the Nuclear Form of Activated Notch 1 Receptor *
TLDR
Data suggest that SEL-10 is involved in shutting off Notch signaling by ubiquitin-proteasomemediated degradation of the active transcriptional factor after a nuclear phosphorylation event.
Phosphorylation of Ser2078 Modulates the Notch2 Function in 32D Cell Differentiation*
TLDR
The results show that the granulocyte colony-stimulating factor stimulation of 32D cells expressing the intracellular Notch2 protein induces phosphorylation at specific sites of this molecule, rendering the molecule inactive and permitting differentiation of these cells, and indicates that Ser2078 is a critical residue for phosphorylated and modulation of Notch 2 activity in the context of G-CSF-induced differentiation of 32 D cells.
Role of glycogen synthase kinase 3 beta as a negative regulator of dorsoventral axis formation in Xenopus embryos.
TLDR
It is strongly suggested that XGSK-3 beta functions to inhibit dorsoventral axis formation in the embryo and evidence for conservation of the Wnt signaling pathway in Drosophila and vertebrates is provided.
...
1
2
3
4
5
...