ArticleProceedings of the National Academy of Sciences of the United States of America2007
Regulation of Alzheimer's disease amyloid-beta formation by casein kinase I.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Genome-wide association study of brain amyloid deposition as measured by Pittsburgh Compound-B (PiB)-PET imaging.Molecular psychiatry · 2021Pooled it
- Rationally Designed Dual Kinase Inhibitors for Management of Obstructive Sleep Apnea-A Computational Study.Biomedicines · 2026Article
- Molecular mechanisms and consequences of TDP-43 phosphorylation in neurodegeneration.Molecular neurodegeneration · 2025Review
- Protein kinases in neurodegenerative diseases: current understandings and implications for drug discovery.Signal transduction and targeted therapy · 2025Review
- Exploring New Structures of Kinase Inhibitors and Multitarget Strategies in Alzheimer's Disease Treatment.Protein and peptide letters · 2025Review
- CK and LRRK2 Involvement in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Targeting sleep and the circadian system as a novel treatment strategy for Parkinson's disease.Journal of neurology · 2024Article
- Fighting Against the Clock: Circadian Disruption and Parkinson's Disease.Journal of movement disorders · 2024Article
- Thermal proteome profiling unveils protein targets of deoxycholic acid in living neuronal cells.Advanced biotechnology · 2023Article
- Circadian disruption and sleep disorders in neurodegeneration.Translational neurodegeneration · 2023Review
- The protein kinase CK1: Inhibition, activation, and possible allosteric modulation.Frontiers in molecular biosciences · 2022Review
- CK2 and protein kinases of the CK1 superfamily as targets for neurodegenerative disorders.Frontiers in molecular biosciences · 2022Review
- Recent Advances on Functional Nucleic-Acid Biosensors.Sensors (Basel, Switzerland) · 2021Review
- Presenilin 1 phosphorylation regulates amyloid-β degradation by microglia.Molecular psychiatry · 2021Article
- A Computational Workflow for the Identification of Novel Fragments Acting as Inhibitors of the Activity of Protein Kinase CK1δ.International journal of molecular sciences · 2021Article
- Tau Protein Interaction Partners and Their Roles in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2021Review
- Cationic Polythiophene-based Colorimetric Assay for Probing the Activity of Protein Kinase A.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2021Article
- CK1δ-Derived Peptides as Novel Tools Inhibiting the Interactions between CK1δ and APP695 to Modulate the Pathogenic Metabolism of APP.International journal of molecular sciences · 2021Article
- Functions and regulation of the serine/threonine protein kinase CK1 family: moving beyond promiscuity.The Biochemical journal · 2020Review
- CK1δ over-expressing mice display ADHD-like behaviors, frontostriatal neuronal abnormalities and altered expressions of ADHD-candidate genes.Molecular psychiatry · 2020Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is associated with accumulation of the neurotoxic peptide amyloid-beta (Abeta), which is produced by sequential cleavage of amyloid precursor protein (APP) by the aspartyl protease beta-secretase and the presenilin-dependent protease gamma-secretase. An increase of casein kinase 1 (CK1) expression has been described in the human AD brain. We show, by using in silico analysis, that APP, beta-secretase, and gamma-secretase subunits contain, in their intracellular regions, multiple CK1 consensus phosphorylation sites, many of which are conserved among human, rat, and mouse species. Overexpression of constitutively active CK1epsilon, one of the CK1 isoforms expressed in brain, leads to an increase in Abeta peptide production. Conversely, three structurally dissimilar CK1-specific inhibitors significantly reduced endogenous Abeta peptide production. By using mammalian cells expressing the beta C-terminal fragment of APP, it was possible to demonstrate that CK1 inhibitors act at the level of gamma-secretase cleavage. Importantly, Notch cleavage was not affected. Our results indicate that CK1 represents a therapeutic target for prevention of Abeta formation in AD.
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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.