Glycogen synthase kinase-3&bgr; is highly activated in nuclei and mitochondria

@article{Bijur2003GlycogenSK,
  title={Glycogen synthase kinase-3\&bgr; is highly activated in nuclei and mitochondria},
  author={Gautam N. Bijur and Richard Scott Jope},
  journal={NeuroReport},
  year={2003},
  volume={14},
  pages={2415-2419}
}
  • G. Bijur, R. Jope
  • Published 19 December 2003
  • Biology, Computer Science
  • NeuroReport
Glycogen synthase kinase-3&bgr; (GSK3&bgr;) is located predominantly in the cytosol, but also is in nuclei and mitochondria. In SH-SY5Y cells, primary cortical neurons, and mouse brain, the portion of active GSK3&bgr; (not phosphorylated on serine-9) was 5- to 8-fold greater in nuclei and mitochondria than in cytosol. Correspondingly greater GSK3&bgr; activities were measured in nuclei and mitochondria compared with cytosol. Stimulation of apoptotic signaling by treatment with camptothecin or… 
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TLDR
It is shown that short hairpin RNA (shRNA) knockdown of GSK-3β, but not G SK-3α, protects cerebellar granule neurons from trophic-deprivation-induced death.
Mitochondrial Hexokinase II Promotes Neuronal Survival and Acts Downstream of Glycogen Synthase Kinase-3*
TLDR
It is demonstrated that chronic inhibition of GSK-3 reprograms the metabolism of neuronal cells, leading to an enhancement of glycolysis, and HKII overexpression is sufficient to protect against rotenone-induced cell death, and mitochondrial HKII is a promoter of neuronal survival under the regulation of G SK-3.
Glycogen synthase kinase-3 is involved in the regulation of the cell cycle in cerebellar granule cells
Resolution of the Nuclear Localization Mechanism of Glycogen Synthase Kinase-3
TLDR
This mechanism is resolved by identifying a bipartite nuclear localization sequence (NLS) that is necessary for the nuclear accumulation of GSK3β and is sufficient to drive yellow fluorescent protein into the nucleus and found that the antiapoptotic effect of G SK3β in tumor necrosis factor-induced apoptosis is mediated by cytosolic, not nuclear, GSK2β.
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.
The Key Roles of GSK-3β in Regulating Mitochondrial Activity
TLDR
Accumulative evidence demonstrates that GSK-3β inactivation may be potentially developed as the promising strategy in management of many diseases, such as Alzheimer’s disease (AD) and Parkinson's disease (PD).
Inhibition of glycogen synthase kinase-3 protects cells from intrinsic but not extrinsic oxidative stress
TLDR
Glycogen synthase kinase-3 is an important component of intrinsic oxidative stress-induced apoptosis that acts downstream of mitochondrial Bax activation, and there are substantial differences in the role of glycogen synthases kinases-3, and lithium's effects, in apoptotic signaling induced by intrinsic and extrinsic oxidative stress.
Glycogen Synthase Kinase-3 (GSK-3)-Targeted Therapy and Imaging
TLDR
The structure, function, expression levels, and ligand-binding properties of GSK-3 and its connection to various diseases are reviewed and a rational perspective and possible route to selective and effective G SKS-3 inhibitors is discussed.
INTRUSION OF GLYCOGEN SYNTHASE KINASE-3Β TO COPE VARIOUS CARDIAC DISORDERS AT MOLECULAR LEVEL
TLDR
GSK-3β is believed to be an imperative target for the discovery and development of newer drugs and their contributory role in cardiac disorders and various other diseases is explored.
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.
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