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Updated: May 17, 2026

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
Published on: April 24, 2021
Signaling pathways involved in endoplasmic reticulum stress-induced neuronal apoptosis
Di Liu1, Mengren Zhang, Hongchao Yin
1Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
Abstract:
In eukaryotic cells, the endoplasmic reticulum (ER) is a very critical site for synthesis, folding, modification of protein, and calcium homeostasis. The ER responds to factors that perturb ER function such as the accumulation of unfolded proteins (ER stress) by activating unfolded protein response to relieve the stress. However, chronic or unresolved ER stress can induce neuronal apoptosis by activating c-Jun N-terminal kinase (JNK), glycogen synthase kinase 3/3β (GSK3/3β), CAAT/enhancer binding protein homologous protein (CHOP), and caspase-12 pathway. Research related to ER stress will provide therapeutic implications in neurological diseases.
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