ArticlePloS one2009
Upregulation of alpha7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- A Novel Regulatory System in Brain Development and Death Driven by a Bioactive Peptide Linked to a Specific Isoform of Acetylcholinesterase.Biomolecules · 2026Article
- A Novel 14mer Peptide Inhibits Autophagic Flux via Selective Activation of the mTORC1 Signalling Pathway: Implications for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- A Novel Peptide Driving Neurodegeneration Appears Exclusively Linked to the α7 Nicotinic Acetylcholine Receptor.Molecular neurobiology · 2024Article
- The human acetylcholinesterase C-terminal T30 peptide activates neuronal growth through alpha 7 nicotinic acetylcholine receptors and the mTOR pathway.Scientific reports · 2023Article
- Article
- A Novel Bioactive Peptide, T14, Selectively Activates mTORC1 Signalling: Therapeutic Implications for Neurodegeneration and Other Rapamycin-Sensitive Applications.International journal of molecular sciences · 2023Article
- Characterization of a Bioactive Peptide T14 in the Human and Rodent Substantia Nigra: Implications for Neurodegenerative Disease.International journal of molecular sciences · 2022Article
- A novel process driving Alzheimer's disease validated in a mouse model: Therapeutic potential.Alzheimer's & dementia (New York, N. Y.) · 2022Article
- Article
- Interacting withActa pharmaceutica Sinica. B · 2020Article
- Natural Peptides in Drug Discovery Targeting Acetylcholinesterase.Molecules (Basel, Switzerland) · 2018Review
- Modulatory Effects of a Novel Cyclized Peptide in Reducing the Expression of Markers Linked to Alzheimer's Disease.Frontiers in neuroscience · 2018Article
- Cancer and neurodegeneration: two sides, same coin?Oncotarget · 2017Article
- A NovelFrontiers in cellular neuroscience · 2017Article
- Decreased neuroinflammation correlates to higher vagus nerve activity fluctuations in near-term ovine fetuses: a case for the afferent cholinergic anti-inflammatory pathway?Journal of neuroinflammation · 2016Article
- Chemical crosslinkers enhance detection of receptor interactomes.Frontiers in pharmacology · 2014Review
- Neuronal AChE splice variants and their non-hydrolytic functions: redefining a target of AChE inhibitors?British journal of pharmacology · 2013Review
- Additive toxicity of β-amyloid by a novel bioactive peptide in vitro: possible implications for Alzheimer's disease.PloS one · 2013Article
- Central nicotinic acetylcholine receptor involved in Ca(2+) -calmodulin-endothelial nitric oxide synthase pathway modulated hypotensive effects.British journal of pharmacology · 2011Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL
findingsThis study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration.
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