ArticleEuropean journal of pharmacology2011
Involvement of notch signaling pathway in amyloid precursor protein induced glial differentiation.
Article in European journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Amyloid Precursor Protein (APP) Regulates Gliogenesis and Neurogenesis of Human Neural Stem Cells by Several Signaling Pathways.International journal of molecular sciences · 2023Article
- Heat Shock Alters the Proteomic Profile of Equine Mesenchymal Stem Cells.International journal of molecular sciences · 2022Article
- The interplay of aryl hydrocarbon receptor/WNT/CTNNB1/Notch signaling pathways regulate amyloid beta precursor mRNA/protein expression and effected the learning and memory of mice.Toxicology research · 2022Article
- Deciphering the neuroprotective and neurogenic potential of soluble amyloid precursor protein alpha (sAPPα).Cellular and molecular life sciences : CMLS · 2020Review
- A systematic simulation-based meta-analytical framework for prediction of physiological biomarkers in alopecia.Journal of biological research (Thessalonike, Greece) · 2019Article
- Physiological effects of amyloid precursor protein and its derivatives on neural stem cell biology and signaling pathways involved.Neural regeneration research · 2019Article
- miR-9 stimulation enhances the differentiation of neural stem cells with zoanthamine by regulating Notch signaling.American journal of translational research · 2019Article
- Role of Amyloid Precursor Protein (APP) and Its Derivatives in the Biology and Cell Fate Specification of Neural Stem Cells.Molecular neurobiology · 2018Review
- Osthole Stimulated Neural Stem Cells Differentiation into Neurons in an Alzheimer's Disease Cell Model via Upregulation of MicroRNA-9 and Rescued the Functional Impairment of Hippocampal Neurons in APP/PS1 Transgenic Mice.Frontiers in neuroscience · 2017Article
- Article
- The amyloid precursor protein (APP) triplicated gene impairs neuronal precursor differentiation and neurite development through two different domains in the Ts65Dn mouse model for Down syndrome.The Journal of biological chemistry · 2013Article
- β-secretase cleavage of the fly amyloid precursor protein is required for glial survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- All in the Family: How the APPs Regulate Neurogenesis.Frontiers in neuroscience · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The amyloid precursor protein (APP) has been mainly studied in its role in the production of amyloid β peptides (Aβ), because Aβ deposition is a hallmark of Alzheimer's disease. Although several studies suggest APP has physiological functions, it is still controversial. We previously reported that APP increased glial differentiation of neural progenitor cells (NPCs). In the current study, NPCs transplanted into APP23 transgenic mice primarily differentiated into glial cells. In vitro treatment with secreted APP (sAPP) dose-dependently increased glial fibrillary acidic protein (GFAP) immuno-positive cells in NPCs and over expression of APP caused most NPCs to differentiate into GFAP immuno-positive cells. Treatment with sAPP also dose-dependently increased expression levels of GFAP in NT-2/D1 cells along with the generation of Notch intracellular domain (NICD) and expression of Hairy and enhancer of split 1 (Hes1). Treatment with γ-secretase inhibitor suppressed the generation of NICD and reduced Hes1 and GFAP expressions. Treatment with the N-terminal domain of APP (APP 1-205) was enough to induce up regulation of GFAP and Hes1 expressions, and application of 22 C11 antibodies recognizing N-terminal APP suppressed these changes by sAPP. These results indicate APP induces glial differentiation of NPCs through Notch signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.