Coupling endoplasmic reticulum stress to the cell death program
By R. Rao, H. Ellerby, Dale E. Bredesen. Cell Death and Differentiation, 2004
1,079 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/fb53843a80dc0b4eaf04e00bcc73b93bc219b824
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Citations in the corpus
- Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “CHOP is induced through the PERK pathway, caspase-12 and JNK signaling are activated, and proapoptotic Bcl-2 proteins BAX and BAK are switched on by the IRE1a pathway (Hetz et al., 2006; Rao et al., 2004).”
- Orchestrating the unfolded protein response in health and disease. (2002, background): “However, APAF1–/– cells are susceptible to ER stress–induced apoptosis, indicating that the mitochondrial pathway is not essential (45).”
- The role of the unfolded protein response in tumour development: friend or foe? (2004, neutral): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&list_uids=840">caspase-7 (Ref”
- CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. (2004, background): “Various downstream effectors of cell death induced by ER stress have been identified (Nakagawa et al. 2000; Rao et al. 2001; Wei et al. 2001); however, the proximal steps that mobilize them during ER stress are poorly understood.”
- Cellular response to endoplasmic reticulum stress: a matter of life or death (2006, background): “For example, ER stress can induce the activation of caspase-9 independent of Apaf-1, the usual mediator of caspase-9 activation.(166) This probably occurs via the direct cleavage of caspase-9 by caspase-12.”
- ER stress and neurodegenerative diseases (2006, background): “Caspase-12 could in turn activate downstream caspases inducing cell death.(22,23) The association of caspase-12 with human”