A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress.
By M. Boyce, Kevin F. Bryant, C. Jousse, Kai Long, H. Harding, D. Scheuner, R. Kaufman, D. Ma, D. Coen, D. Ron and 1 more. Science, 2005
679 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/7322791117d359c63adce5d011a55a24fbb0fd82
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- R. Kaufman
- Junying Yuan
- Y. Kouroku
- M. Boyce
- I. Tanida
- E. Fujita
- Peter Walter
- Mauro Costa-Mattioli
Citations in the corpus
- Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, unknown): “Salubrinal is a small molecule that prevents dephosphorylation of eIF2a (Boyce et al., 2005).”
- The integrated stress response (2016, unknown): “Inhibitors of eIF2 a dephosphorylation include drugs such as salubrinal [223] and guanabenz (2,6-dichlorobenzylidene amino-guanidine acetate) or its derivative Sephin1, which inactivate the binding of GADD34 to PP1c [224 – 226].”
- The integrated stress response: From mechanism to disease (2020, background): “Salubrinal (65) and its more potent and soluble derivative Sal003 (66) inhibit both phosphatase complexes (GADD34•PP1 and CReP•PP1), but their precise mechanism of action remains unclear.”
- Calreticulin exposure dictates the immunogenicity of cancer cell death (2007, unknown): “and salubrinal (which inhibits the PP1/GADD34 complex”
- In brief (2011, unknown): “Salubrinal blocks translation initiation by selective inhibition of eIF2a dephosphorylation (Boyce et al., 2005; Cnop et al., 2007) (Figure S3B).”
- ER stress (PERK/eIF2α phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation (2007, background): “Phosphorylation of eIF2a inhibits ER-stress-induced caspase-12 activation and ER-stress-mediated cells death.(37,38) Cells with phosphorylated eIF2a are resistant to oxidative stress(39) and inhibition of eIF2a dephosphorylation promotes survival of stressed cells.”
- Cellular response to endoplasmic reticulum stress: a matter of life or death (2006, background): “termed salubrinal, can protect cells from ER stress-induced apoptosis.(139) ER stress can also activate well-known general regulators of mammalian apoptosis, including the Bcl-2 and caspase families of proteins.”