ArticleJournal of molecular neuroscience : MN2017
The Involvement of NR2B and tau Protein in MG132-Induced CREB Dephosphorylation.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Identification and mechanistic insights of ubiquitin-proteasome system and pyroptosis-related biomarkers in type 2 diabetes mellitus.World journal of diabetes · 2025Article
- Design, synthesis, and in vitro and in vivo characterization of new memantine analogs for Alzheimer's disease.European journal of medicinal chemistry · 2022Article
- Ferroptosis promotes microtubule-associated protein tau aggregation via GSK-3β activation and proteasome inhibition.Molecular neurobiology · 2022Article
- Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade.Molecular neurodegeneration · 2019Article
- Risk Factors for Alzheimer's Disease: Focus on Stress.Frontiers in pharmacology · 2019Review
- Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade.Journal of Alzheimer's disease : JAD · 2018Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
Transcription factor cAMP response element-binding protein (CREB) plays a critical role in memory formation. Ubiquitin-proteasome system-dependent protein degradation affects the upstream signaling pathways which regulate CREB activity. However, the molecular mechanisms of proteasome inhibition on reductive CREB activity are still unclear. The current study demonstrated that MG132-inhibited proteasome activity resulted in a dose dependence of CREB dephosphorylation at Ser133 as well as decreased phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunit NR2B (Tyr1472) and its tyrosine protein kinase Fyn (Tyr416). These dephosphorylations are probably caused by disturbance of expression and post-translational modifications of tau protein since tau siRNA decreased the activity of Fyn, NR2B, and CREB. To further confirm this perspective, HEK293 cells stably expressing human tau441 protein were treated with MG132 and dephosphorylations of CREB and NR2B were observed. The current research provides an alternative pathway, tau/Fyn/NR2B signaling, regulating CREB activity.
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