ArticleMolecular neurodegeneration2016
The novel RAGE interactor PRAK is associated with autophagy signaling in Alzheimer's disease pathogenesis.
Article in Molecular neurodegeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Relationship between Advanced Glycation End Products and Steroidogenesis in PCOS.Reproductive biology and endocrinology : RB&E · 2016Pooled it
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- Exploring the Shared Genetic Architectures Between Primary Open-Angle Glaucoma and Visual Pathway Regions in the Brain.Investigative ophthalmology & visual science · 2025Article
- Targeting RAGE with Nanobodies for Molecular Imaging of Cancers and Alzheimer's Disease.Advanced biology · 2025Article
- MK5 Regulates Microglial Activation and Neuroinflammation in Experimental Stroke Models.CNS neuroscience & therapeutics · 2025Article
- Exosomes Derived from M2 Microglial Cells Modulated by 1070-nm Light Improve Cognition in an Alzheimer's Disease Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Role and Therapeutic Potential of RAGE Signaling in Neurodegeneration.Current drug targets · 2022Article
- Neuroprotective Effects of Endogenous Secretory Receptor for Advanced Glycation End-products in Brain Ischemia.Aging and disease · 2020Article
- A High Content Screen in Macrophages Identifies Small Molecule Modulators of STING-IRF3 and NFkB Signaling.ACS chemical biology · 2018Article
- Molecular and functional signatures in a novel Alzheimer's disease mouse model assessed by quantitative proteomics.Molecular neurodegeneration · 2018Article
- TREM2 in Alzheimer's Disease: Microglial Survival and Energy Metabolism.Frontiers in aging neuroscience · 2018Article
- PRAK mediates Aβ-RAGE driven autophagy pathway.Oncotarget · 2017Article
- Overexpression of receptor for advanced glycation end products (RAGE) in ovarian cancer.Cancer biomarkers : section A of Disease markers · 2017Article
- Direct interaction of beta-amyloid with Na,K-ATPase as a putative regulator of the enzyme function.Scientific reports · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe receptor for advanced glycation end products (RAGE) has been found to interact with amyloid β (Aβ). Although RAGE does not have any kinase motifs in its cytosolic domain, the interaction between RAGE and Aβ triggers multiple cellular signaling involved in Alzheimer's disease (AD). However, the mechanism of signal transduction by RAGE remains still unknown. Therefore, identifying binding proteins of RAGE may provide novel therapeutic targets for AD.
resultsIn this study, we identified p38-regulated/activated protein kinase (PRAK) as a novel RAGE interacting molecule. To investigate the effect of Aβ on PRAK mediated RAGE signaling pathway, we treated SH-SY5Y cells with monomeric form of Aβ. We demonstrated that Aβ significantly increased the phosphorylation of PRAK as well as the interaction between PRAK and RAGE. We showed that knockdown of PRAK rescued mTORC1 inactivation induced by Aβ treatment and decreased the formation of Aβ-induced autophagosome.
conclusionsWe provide evidence that PRAK plays a critical role in AD pathology as a key interactor of RAGE. Thus, our data suggest that PRAK might be a potential therapeutic target of AD involved in RAGE-mediated cell signaling induced by Aβ.
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