ArticleJournal of biomedical research2024
The roles of RACK1 in the pathogenesis of Alzheimer's disease.
Article in Journal of biomedical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- PKCβII Activation Promotes Membrane-Proximal Enrichment of Ribosome-Bound RACK1.International journal of molecular sciences · 2026Article
- Neuroinflammation and Secretase Regulation in Alzheimer's Disease: From Molecular Cross-Talk to Multi-Target Therapeutics.International journal of molecular sciences · 2026Review
- Temporal- and sex-specific changes in proteasome-dependent and independent polyubiquitination in the amygdala during fear memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2026Article
- Microglial Rack1 Deficiency Alleviates Alzheimer's Disease Pathology through Enhancing IGF1-Mediated Astrocytic Phagocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Proteome Microarray-Guided Global View: Multiple Pharmacological Targets of Icariin.Drug design, development and therapy · 2026Article
- A Duality of Function: An Integrative Model of RACK1 as a Switch Between Translational and Signaling Hubs.International journal of molecular sciences · 2025Review
- Endocrine Disrupting Toxicity of Bisphenol A and Its Analogs: Implications in the Neuro-Immune Milieu.Journal of xenobiotics · 2025Review
- Insights into the regulation of mRNA translation by scaffolding proteins.Biochemical Society transactions · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The receptor for activated C kinase 1 (RACK1) is a protein that plays a crucial role in various signaling pathways and is involved in the pathogenesis of Alzheimer's disease (AD), a prevalent neurodegenerative disease. RACK1 is highly expressed in neuronal cells of the central nervous system and regulates the pathogenesis of AD. Specifically, RACK1 is involved in regulation of the amyloid-β precursor protein processing through α- or β-secretase by binding to different protein kinase C isoforms. Additionally, RACK1 promotes synaptogenesis and synaptic plasticity by inhibiting N-methyl-D-aspartate receptors and activating gamma-aminobutyric acid A receptors, thereby preventing neuronal excitotoxicity. RACK1 also assembles inflammasomes that are involved in various neuroinflammatory pathways, such as nuclear factor-kappa B, tumor necrosis factor-alpha, and NOD-like receptor family pyrin domain-containing 3 pathways. The potential to design therapeutics that block amyloid-β accumulation and inflammation or precisely regulate synaptic plasticity represents an attractive therapeutic strategy, in which RACK1 is a potential target. In this review, we summarize the contribution of RACK1 to the pathogenesis of AD and its potential as a therapeutic target.
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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.