scholarly journals Nerve Growth Factor (NGF) Regulates Activity of Nuclear Factor of Activated T-cells (NFAT) in Neurons via the Phosphatidylinositol 3-Kinase (PI3K)-Akt-Glycogen Synthase Kinase 3β (GSK3β) Pathway

2014 ◽  
Vol 289 (45) ◽  
pp. 31349-31360 ◽  
Author(s):  
Man-Su Kim ◽  
Leonid P. Shutov ◽  
Aswini Gnanasekaran ◽  
Zhihong Lin ◽  
Jacob E. Rysted ◽  
...  
Keyword(s):  
T Cells ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Nuclear Factor ◽  
Glycogen Synthase Kinase 3Β ◽  
Phosphatidylinositol 3 Kinase ◽  
Activated T Cells ◽  
Nerve Growth

scholarly journals Activation of Casein Kinase II and Inhibition of Phosphatase and Tensin Homologue Deleted on Chromosome 10 Phosphatase by Nerve Growth Factor/p75NTR Inhibit Glycogen Synthase Kinase-3β and Stimulate Axonal Growth

2006 ◽  
Vol 17 (8) ◽  
pp. 3369-3377 ◽  
Author(s):  
María-Angeles Arevalo ◽  
Alfredo Rodríguez-Tébar
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Glycogen Synthase ◽  
Casein Kinase Ii ◽  
Casein Kinase ◽  
Glycogen Synthase Kinase ◽  
Chromosome 10 ◽  
Nerve Growth ◽  
Gsk 3Β ◽  
Phosphatase And Tensin Homologue

Axonal elongation and guidance are controlled by extracellular factors such as the neurotrophins. Indeed, nerve growth factor (NGF) seems to promote axon growth through binding to its p75NTR receptor and inactivating RhoA. Furthermore, the local inhibition of glycogen synthase kinase (GSK)-3β by NGF also favors microtubule polymerization and axon extension. Inactivation of GSK-3β may be due to the NGF/TrkA-mediated activation of phosphatidylinositol-3 kinase (PI-3 kinase), which increases the levels of phosphatydilinositol 3-phosphate [PI(3)P]. However, we show here that NGF may inactivate GSK-3β through an alternative mechanism. In cultured hippocampal neurons, the capacity of NGF to promote axon elongation is mostly mediated by p75NTR, and the activation of this pathway leads to the inactivation of GSK-3β. However, the signaling pathway triggered by NGF/p75NTR acts through casein kinase II (CK2). NGF/p75NTR-activated CK2 phosphorylates the phosphatase and tensin homologue deleted on chromosome 10 (PTEN), thus rendering this phosphatase inactive. Like activation of the PI-3 kinase, PTEN inactivation allows PI(3)P levels to increase, thus favoring GSK-3β inactivation and axon outgrowth. This newly disclosed mechanism may help to extend the repertoire of pharmacological agents that activate CK2 or that inhibit PTEN to stimulate axon regeneration after trauma or disease.

scholarly journals Lithium regulates keratinocyte proliferation via glycogen synthase kinase 3 and NFAT2 (nuclear factor of activated T cells 2)

2012 ◽  
Vol 227 (4) ◽  
pp. 1529-1537 ◽  
Author(s):  
Philip J. Hampton ◽  
Ralph Jans ◽  
Ross J. Flockhart ◽  
Graeme Parker ◽  
Nick J. Reynolds
Keyword(s):  
T Cells ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3 ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Keratinocyte Proliferation

Glycogen synthase kinase-3β is critical for Interferon-α-induced serotonin uptake in human Jurkat T cells

2012 ◽  
Vol 227 (6) ◽  
pp. 2556-2566 ◽  
Author(s):  
Chiung-Wen Tsao ◽  
Chiou-Feng Lin ◽  
Hung-Tsung Wu ◽  
Ching-Ting Ma ◽  
Wei-Ching Huang ◽  
...  
Keyword(s):  
T Cells ◽  
Glycogen Synthase ◽  
Serotonin Uptake ◽  
Glycogen Synthase Kinase ◽  
Interferon Α ◽  
Glycogen Synthase Kinase 3Β ◽  
Jurkat T Cells
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