PERK inhibition mitigates acrylamide-induced tau phosphorylation and synaptic deficits via the GSK-3β and ATF4 pathways in human neuroblastoma SH-SY5Y cells.
📄 Abstract
Acrylamide (ACR), a potential neurotoxin prevalent in carbohydrate-rich foods, poses a significant public health concern. While ACR exposure is known to induce tau phosphorylation and synaptic impairment, the underlying mechanisms remain incompletely understood. The aberrant activation of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-eukaryotic initiation factor-2α (eIF2α) signaling pathway is emerging as a major common theme in neurodegenerative disorders. This study investigated the role of the PERK-eIF2α signaling pathway in ACR-induced neurotoxicity using human neuroblastoma SH-SY5Y cells. Our results showed that ACR exposure not only significantly increased tau phosphorylation at specific epitopes (Ser
Confidence:
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· 6 полей извлечено
Идентификация (6 полей)
Target
PERK
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Alt. target
protein kinase RNA-like endoplasmic reticulum kinase
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Protein family
eIF2α kinase family
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Functional class
kinase
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Subcellular loc.
endoplasmic reticulum
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Isoforms (metab/obesity)
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Механизм действия (21 полей)
Mechanism
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Mutations (obesity/lean)
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Activity (obesity)
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Activity temporal
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Energy balance
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Appetite
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Fat metabolism
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Lipolysis
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Thermogenesis
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Muscle metabolism
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Inflammation
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Glucose metabolism
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AA metabolism
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Hormonal pathways
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Cell death
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Adipocyte fibrosis
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Upstream (biochem)
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Upstream (physiol)
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Downstream (biochem)
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Downstream (physiol)
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PTMs
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Экспрессия (8 полей)
Tissue expression
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In vitro
human neuroblastoma SH-SY5Y cells
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In vivo
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Ex vivo
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