Nitric oxide-induced apoptosis in pancreatic β cells is mediated by the endoplasmic reticulum stress pathway

By S. Oyadomari, K. Takeda, M. Takiguchi, T. Gotoh, M. Matsumoto, I. Wada, Shizuo Akira, E. Araki, M. Mori. Proceedings of the National Academy of Sciences of the United States of America, 2001

600 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Surgery

View Paper: https://www.semanticscholar.org/paper/6b0374a84aec8e32b7c378cf84ce3cd9cf112490

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In Cell Biology

1. John Calvin Reed
2. M. Cnop
3. Jonathan H. Lin
4. Peter Walter
5. T. Yen
6. S. Oyadomari
7. A. K. Cardozo
8. Inki Kim

In Genetics

1. M. Cnop
2. F. Ortis
3. Shizuo Akira
4. Decio L. Eizirik
5. R. Kaufman
6. G. Hotamışlıgil
7. D. Ron

In Surgery

1. M. Cnop
2. John Calvin Reed
3. F. Ortis
4. Peter Walter
5. Jonathan H. Lin
6. Shizuo Akira
7. Decio L. Eizirik
8. R. Kaufman

Citations in the corpus

• Endoplasmic reticulum stress in disease pathogenesis. (2008, background): “Cytokines and nitric oxide released by the inflammatory cells have been shown to activate the UPR, presumably by inducing ER stress (58, 59).”
• The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “The chemical NO donor SNAP depletes ER Ca(2) in MIN-6 cells (180).”
• A review of soil NO transformation: associated processes and possible physiological significance on organisms (2015, background): “…of NO Endocrine system Oyadomari et al., 2002 Apoptosis due to eliminating Ca2+ from endoplasmic reticulum Overproduction of NO Pancreatic β- cells Oyadomari et al., 2001, 2002 Damaging DNA, proteins and lipids NO-mediated oxidative reaction products (e.g. ONOO-) Various types of cells Lee et…”
• Initiation and execution of lipotoxic ER stress in pancreatic β-cells (2008, background): “Role of ATF3 and CHOP in FFA-induced β-cell apoptosis Because of the prominent induction of ATF3 and CHOP by palmitate in clonal β-cells, and in rat and human primary β-cells (Figs 3 and 5), and their role in ER-stress-induced cell death (Hartman et al., 2004; Oyadomari et al., 2001), we examined wh”
• Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes. (2002, methodology): “Mouse insulinoma MIN6 cells were cultured in 60-mm collagen-coated dishes in DMEM supplemented with 25 mM glucose and 10% FCS, as described (11).”
• Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Pancreatic β-cell apoptosis induced by NO, a mediator of inflammation of relevance to autoimmune (type 1) diabetes, has been shown to be CHOP-dependent, which further implicates ER stress as an instigator of β-cell deat”