title: Signaling pathways involved in endoplasmic reticulum stress-induced neuronal apoptosis.
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.
authors.affiliation: Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
authors.forename: Di
authors.initials: D
authors.lastname: Liu
authors.forename: Mengren
authors.initials: M
authors.lastname: Zhang
authors.forename: Hongchao
authors.initials: H
authors.lastname: Yin
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D004721:Endoplasmic Reticulum / Q000502:physiology*; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D006801:Humans; D009474:Neurons / Q000166:cytology / Q000473:pathology* / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*