Results 41 to 50 of about 33,200 (128)

IL-33 suppresses GSK-3β activation through an ST2-independent MyD88/TRAF6/RIP/PI3K/Akt pathway

open access: yesHeliyon, 2018
Aims: The present study was conducted to explore the effect of interleukin-33 (IL-33) on glycogen synthase kinase-3β (GSK-3β) activation involving Tau phosphorylation, a critical causative factor for Alzheimer's disease (AD).
Tomoyuki Nishizaki
doaj   +1 more source

Brief Review of the Role of Glycogen Synthase Kinase-3β in Amyotrophic Lateral Sclerosis

open access: yesNeurology Research International, 2011
Glycogen synthase kinase-3β (GSK-3β) is known to affect a diverse range of biological functions controlling gene expression, cellular architecture, and apoptosis.
Seong-Ho Koh, Wonki Baek, Seung H. Kim
doaj   +1 more source

Drug Development Targeting the Glycogen Synthase Kinase-3β (GSK-3β)-Mediated Signal Transduction Pathway: The Role of GSK-3β in the Maintenance of Steady-State Levels of Insulin Receptor Signaling Molecules and Nav1.7 Sodium Channel in Adrenal Chromaffin Cells

open access: yesJournal of Pharmacological Sciences, 2009
Glycogen synthase kinase-3 (GSK-3) is constitutively active in nonstimulated cells, where the majority of its substrates undergo inactivation/proteolysis by phosphorylation.
Takayuki Nemoto   +3 more
doaj   +1 more source

GSK-3β Contributes to Parkinsonian Dopaminergic Neuron Death: Evidence From Conditional Knockout Mice and Tideglusib

open access: yesFrontiers in Molecular Neuroscience, 2020
Glycogen synthase kinase-3 (GSK-3) dysregulation has been implicated in nigral dopaminergic neurodegeneration, one of the main pathological features of Parkinson’s disease (PD).
Junyu Li   +17 more
doaj   +1 more source

Loss of biliverdin reductase-A favors Tau hyper-phosphorylation in Alzheimer's disease

open access: yesNeurobiology of Disease, 2019
Hyper-active GSK-3β favors Tau phosphorylation during the progression of Alzheimer's disease (AD). Akt is one of the main kinases inhibiting GSK-3β and its activation occurs in response to neurotoxic stimuli including, i.e., oxidative stress.
Nidhi Sharma   +9 more
doaj   +1 more source

Glycogen synthase kinase-3β inactivation inhibits tumor necrosis factor-α production in microglia by modulating nuclear factor κB and MLK3/JNK signaling cascades

open access: yesJournal of Neuroinflammation, 2010
Background Deciphering the mechanisms that modulate the inflammatory response induced by microglial activation not only improves our insight into neuroinflammation but also provides avenues for designing novel therapies that could halt inflammation ...
Chen Wu-Fu   +4 more
doaj   +1 more source

Extracellular α-synuclein leads to microtubule destabilization via GSK-3β-dependent Tau phosphorylation in PC12 cells. [PDF]

open access: yesPLoS ONE, 2014
α-Synuclein (ASN) plays an important role in pathogenesis of Parkinson's disease (PD) and other neurodegenerative disorders. Novel and most interesting data showed elevated tauopathy in PD and suggested relationship between ASN and Tau protein.
Magdalena Gąssowska   +5 more
doaj   +1 more source

Stabilization of mismatch repair gene PMS2 by glycogen synthase kinase 3β is implicated in the treatment of cervical carcinoma

open access: yesBMC Cancer, 2010
Background PMS2 expression loss was reported in a variety of human. However, its importance has not been fully understood in cervical carcinoma. The aim of this study was to determine the expression of PMS2 in cervical carcinoma and evaluate the ...
Wang Ze   +5 more
doaj   +1 more source

GSK-3β and Memory Formation

open access: yesFrontiers in Molecular Neuroscience, 2012
In Alzheimer’s disease (AD), tau hyperphosphorylation and neurofibrillary tangle (NFT) formation are strongly associated with dementia. Memory impairment is a characteristic, early symptom of AD.
Akihiko eTakashima
doaj   +1 more source

Ketamine modulates disrupted in schizophrenia-1/glycogen synthase kinase-3β interaction

open access: yesFrontiers in Molecular Neuroscience
IntroductionDisrupted in schizophrenia-1 (DISC1) is a scaffolding protein whose mutated form has been linked to schizophrenia, bipolar affective disorders, and recurrent major depression.
Jia-Ren Liu   +5 more
doaj   +1 more source

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