An integrated stress response regulates amino acid metabolism and resistance to oxidative stress.

By H. Harding, Yuhong Zhang, H. Zeng, I. Novoa, Phoebe D. Lu, M. Calfon, Navid Sadri, Chi Y. Yun, B. Popko, R. Paules and 5 more. Molecules and Cells, 2003

3,280 citations recorded by the source corpus.

Subfields: Cell Biology, Physiology, Rehabilitation

View Paper: https://www.semanticscholar.org/paper/0768a85411a0fcbb8c68dd38377453c66f82e23e

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In Cell Biology

1. R. Kaufman
2. C. Hetz
3. G. Hotamışlıgil
4. D. Ron
5. J. Malhotra
6. Laurie H. Glimcher
7. Peter Walter
8. Afshin Samali

In Physiology

1. R. Kaufman
2. Donna D. Zhang
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4. K. Davies
5. H. Forman
6. R. Yadav
7. A. Mellor
8. H. Chae

Citations in the corpus

• The endoplasmic reticulum and the unfolded protein response. (2007, background): “Paradoxically, eIF2α phosphorylation induces translation of ATF4 mRNA.”
• The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “Research shows that PERKand ATF4cells and eIF2α (Ser51Ala) knock-in cells fail to induce CHOP during ER stress (32).”
• Translation reinitiation at alternative open reading frames regulates gene expression in an integrated stress response (2004, background): “The low basal expression of NPTII in cells transfected with the uORF1-GFP is a reproducible if unexplained finding. on A ugust 18, 2017 jcb.rupress.org D ow nloaded from CONTROL OF THE ISR • LU ET AL.”
• The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation (2010, background): “Our studies show that inhibition of ATF4 in the absence of any stress, sensitizes tumour cells to NEAA deprivation, a result that is consistent with earlier studies performed in MEFs (Harding et al, 2003).”
• Degradation of misfolded proteins prevents ER-derived oxidative stress and cell death. (2004, background): “Two recent reports have linked ER metabolism with the genTo determine if ERO1 overexpression, uncoupled from UPR regulated expression, could contribute to ROS aceration of reactive oxygen species (ROS) through oxidative protein folding (Harding et al., 2003; Tu and Weiss- cumulation, ERO1 was placed”
• Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival (2003, background): “Previous models for the regulation of Nrf2/Keap1 dissociation have focused on the possibility that ROS promote complex dissociation (46).”
• Translational control in stress and apoptosis (2005, background): “This upregulation is crucial for the UPR, in that ATF4 transcriptionally activates UPR-responsive genes, which encode proteins that ameliorate the ER stres”
• A trip to the ER: coping with stress. (2004, background): “UPR activation also upregulates genes that help with maintaining the redox balance in the cell to both offset the generation of reactive oxygen species owing to ER stress and promote cell survival [ 23 ].”
• NRF2, a Transcription Factor for Stress Response and Beyond (2020, background): “NRF2 activates the transcription of ATF4, which has been linked to amino acid metabolism and resistance to oxidative stress [88,99].”