ReviewNeurochemical research2003
Protein phosphorylation and APP metabolism.
Review in Neurochemical research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 71 citations in OpenAlex.
- Comparing In vitro Protein Aggregation Modelling Using Strategies Relevant to Neuropathologies.Cellular and molecular neurobiology · 2025Article
- Revisiting APP secretases: an overview on the holistic effects of retinoic acid receptor stimulation in APP processing.Cellular and molecular life sciences : CMLS · 2022Review
- High-frequency (50 Hz) electroacupuncture ameliorates cognitive impairment in rats with amyloid beta 1-42-induced Alzheimer's disease.Neural regeneration research · 2018Article
- Altered protein phosphorylation as a resource for potential AD biomarkers.Scientific reports · 2016Article
- Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.Molecular neurobiology · 2015Review
- Complexing Aβ prevents the cellular anomalies induced by the Peptide alone.Journal of molecular neuroscience : MN · 2014Article
- Flavonoids as therapeutic compounds targeting key proteins involved in Alzheimer's disease.ACS chemical neuroscience · 2014Review
- Article
- Effects of nerve growth factor and nitric oxide synthase inhibitors on amyloid precursor protein mRNA levels and protein stability.The open biochemistry journal · 2012Article
- Protein phosphatases and Alzheimer's disease.Progress in molecular biology and translational science · 2012Review
- Neurodegeneration in Alzheimer disease: role of amyloid precursor protein and presenilin 1 intracellular signaling.Journal of toxicology · 2012Article
- Regulation of β cleavage of amyloid precursor protein.Neuroscience bulletin · 2010Review
- Role of Glycogen Synthase Kinase-3β in APP Hyperphosphorylation Induced by NMDA Stimulation in Cortical Neurons.Pharmaceuticals (Basel, Switzerland) · 2010Article
- In AbetaPP-overexpressing cultured human muscle fibers proteasome inhibition enhances phosphorylation of AbetaPP751 and GSK3beta activation: effects mitigated by lithium and apparently relevant to sporadic inclusion-body myositis.Journal of neurochemistry · 2010Article
- Enhanced generation of Alzheimer's amyloid-beta following chronic exposure to phorbol ester correlates with differential effects on alpha and epsilon isozymes of protein kinase C.Journal of neurochemistry · 2009Article
- Pin1 in Alzheimer's disease: multiple substrates, one regulatory mechanism?Biochimica et biophysica acta · 2007Review
- Protein phosphatase 2A methyltransferase links homocysteine metabolism with tau and amyloid precursor protein regulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Neuroprotective effects of regulators of the glycogen synthase kinase-3beta signaling pathway in a transgenic model of Alzheimer's disease are associated with reduced amyloid precursor protein phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Tyr687 dependent APP endocytosis and Abeta production.Journal of molecular neuroscience : MN · 2007Article
- Signal transduction therapeutics: relevance for Alzheimer's disease.Journal of molecular neuroscience : MN · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous lines of evidence place signal transduction cascades at the core of many processes having a direct role in neurodegeneration and associated disorders. Key players include neurotransmitters, growth factors, cytokines, hormones, and even binding and targeting proteins. Indeed, abnormal phosphorylation of key control proteins has been detected in many cases and is thought to underlie the associated cellular dysfunctions. Several signaling cascades have been implicated, affecting processes as varied as protein processing, protein expression, and subcellular protein localization, among others. The Alzheimer's amyloid precursor protein (APP) is a phosphoprotein, with well-defined phosphorylation sites but whose function is not clearly understood. The factors and pathways regulating the processing of APP have been particularly elusive, both in normal ageing and the Alzheimer's disease (AD) condition. Not surprisingly, the physiological function(s) of the protein remain(s) to be elucidated, although many hypotheses have been advanced. Nonetheless, considerable data has accumulated over the last decade, placing APP in key positions to be modulated both directly and indirectly by phosphorylation and phosphorylation-dependent events. The pathological end product of APP processing is the main proteinaceous component of the hallmark senile plaques found in the brains of AD patients, that is, a toxic peptide termed Abeta. In this minireview we address the importance of phosphorylation and signal transduction cascades in relation to APP processing and Abeta production. The possible use of the identified molecular alterations as therapeutic targets is also addressed.
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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.