Requirement for glycogen synthase kinase-3β in cell survival and NF-κB activation

@article{Hoeflich2000RequirementFG,
  title={Requirement for glycogen synthase kinase-3$\beta$ in cell survival and NF-$\kappa$B activation},
  author={Klaus P. Hoeflich and Juan Luo and Elizabeth A. Rubie and Ming-Sound Tsao and Ou Jin and James R. Woodgett},
  journal={Nature},
  year={2000},
  volume={406},
  pages={86-90}
}
Glycogen synthase kinase-3 (GSK-3)-α and -β are closely related protein-serine kinases, which act as inhibitory components of Wnt signalling during embryonic development and cell proliferation in adult tissues. Insight into the physiological function of GSK-3 has emerged from genetic analysis in Drosophila, Dictyostelium and yeast. Here we show that disruption of the murine GSK-3β gene results in embryonic lethality caused by severe liver degeneration during mid-gestation, a phenotype… 
Glycogen Synthase Kinase 3β Functions To Specify Gene-Specific, NF-κB-Dependent Transcription
TLDR
GSK-3β has profound effects on transcription in a gene-specific manner through a mechanism involving control of promoter-specific recruitment of NF-κB.
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.
Glycogen Synthase Kinase-3β Participates in Nuclear Factor κB–Mediated Gene Transcription and Cell Survival in Pancreatic Cancer Cells
TLDR
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The Wnt Pool of Glycogen Synthase Kinase 3β Is Critical for Trophic-Deprivation-Induced Neuronal Death
TLDR
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Glycogen Synthase Kinase 3β-Mediated Apoptosis of Primary Cortical Astrocytes Involves Inhibition of Nuclear Factor κB Signaling
TLDR
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Genetic Deletion of Glycogen Synthase Kinase-3β Abrogates Activation of IκBα Kinase, JNK, Akt, and p44/p42 MAPK but Potentiates Apoptosis Induced by Tumor Necrosis Factor*
TLDR
The results indicate that GSK-3β plays a critical role in TNF signaling and in the signaling of other inflammatory stimuli and that its suppression can be exploited as a potential target to inhibit angiogenesis, proliferation, and survival of tumor cells.
Glycogen Synthase Kinase-3 regulates multiple myeloma cell growth and bortezomib-induced cell death
TLDR
RNA interference experiments showed that in MM cells GSK-3α and β play distinct roles in cell survival and modulate the sensitivity to proteasome inhibitors, and Interestingly, bortezomib caused a reduction of Gsk-3 serine phosphorylation and its nuclear accumulation with a mechanism that resulted partly dependent on G SKS-3 itself.
Differential Roles of Glycogen Synthase Kinase-3 Isoforms in the Regulation of Transcriptional Activation*
TLDR
This work used GSK-3 isoform-specific small interfering RNAs, dominant negative mutants, and pharmacological inhibitors to search for the differential roles in regulating transcriptional activation in cultured rat cerebral cortical neurons to underscore critical variations in the function and regulation of G SKK-3α and G SK-3β.
Glycogen synthase kinase-3β is a crucial mediator of signal-induced RelB degradation
TLDR
It is concluded that GSK-3β is a crucial regulator of RelB degradation, stressing the relevant linkage between the NF-κB system and GSK -3β.
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