ArticleJournal of molecular neuroscience : MN2009
Alphabeta hinders nuclear targeting of AICD and Fe65 in primary neuronal cultures.
Article in Journal of molecular neuroscience : MN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer's Disease.Molecules (Basel, Switzerland) · 2020Review
- RIP at the Synapse and the Role of Intracellular Domains in Neurons.Neuromolecular medicine · 2020Review
- WWOX Phosphorylation, Signaling, and Role in Neurodegeneration.Frontiers in neuroscience · 2018Review
- Impact of Cytokines and Chemokines on Alzheimer's Disease Neuropathological Hallmarks.Current Alzheimer research · 2017Review
- Altered protein phosphorylation as a resource for potential AD biomarkers.Scientific reports · 2016Article
- New cosurface capacitive stimulators for the development of active osseointegrative implantable devices.Scientific reports · 2016Article
- Complexing Aβ prevents the cellular anomalies induced by the Peptide alone.Journal of molecular neuroscience : MN · 2014Article
- Relationships between the amyloid precursor protein and its various proteolytic fragments and neuronal systems.Alzheimer's research & therapy · 2012Article
- The role of APP proteolytic processing in lipid metabolism.Experimental brain research · 2012Review
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Authors and funding
4 authors.
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Abstract
The intracellular domain of the Alzheimer's amyloid precursor protein (AICD) has been described as an important player in the transactivation of specific genes. It results from proteolytic processing of the Alzheimer's amyloid precursor protein (APP), as does the neurotoxic Abeta peptide. Although normally produced in cells, Abeta is typically considered to be a neurotoxic peptide, causing devastating effects. By exposing primary neuronal cultures to relatively low Abeta concentrations, this peptide was shown to affect APP processing. Our findings indicate that APP C-terminal fragments are increased with concomitant reduction in the expression levels of APP itself. AICD nuclear immunoreactivity detected under control conditions was dramatically reduced in response to Abeta exposure. Additionally, intracellular protein levels of Fe65 and GSK3 were also decreased in response to Abeta. APP nuclear signaling is altered by Abeta, affecting not only AICD production but also its nuclear translocation and complex formation with Fe65. In effect, Abeta can trigger a physiological negative feedback mechanism that modulates its own production.
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