Translational control is required for the unfolded protein response and in vivo glucose homeostasis.

By D. Scheuner, B. Song, E. McEwen, Chuan-Yin Liu, R. Laybutt, P. Gillespie, T. Saunders, S. Bonner-Weir, R. Kaufman. Molecules and Cells, 2001

1,413 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/901f2545d41a75685d32b23d3ebd1fb1c2a580e2

How researchers see this paper

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In Cell Biology

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

In Molecular Biology

1. R. Kaufman
2. G. Hotamışlıgil
3. D. Ron
4. C. Hetz
5. J. Malhotra
6. Laurie H. Glimcher
7. M. Schröder
8. H. Harding

In Surgery

1. R. Kaufman
2. G. Hotamışlıgil
3. D. Ron
4. J. Malhotra
5. Peter Walter
6. S. S. Cao
7. Laurie H. Glimcher
8. E. Gilbert

Citations in the corpus

• Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease (2014, background): “increases apoptosis in pancreatic  cells (67,147).”
• IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA (2002, background): “UPR gene expression in mammals relies largely on pancreatic ER kinase (PERK) and ATF6 (ref”
• ER stress: Autophagy induction, inhibition and selection (2015, background): “Genes encoding DDIT3 contain promoter-binding sites for transcription factors from all 3 branches of the UPR, ATF4, ATF6, and XBP1.”
• Nutrient sensing and inflammation in metabolic diseases (2008, background): “Furthermore, UPR signalling, particularly the PERK-mediated branch of this response, has a role in the maintenance of glucose homeostasis, and activation of the UPR is required for withstanding glucose or energy fluctuations in cells, especially pancreatic β-cells and plasma cells”
• Adaptation to ER Stress Is Mediated by Differential Stabilities of Pro-Survival and Pro-Apoptotic mRNAs and Proteins (2006, methodology): “Total radioactivity was measured by TCA (trichloroacetic acid) precipitation on a filter [20].”
• An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. (2003, background): “A sig2001; Scheuner et al., 2001).”
• Translational Repression Mediates Activation of Nuclear Factor Kappa B by Phosphorylated Translation Initiation Factor 2 (2004, background): “The two known examples of this involve the yeast transcription factor GCN4 (19) and the mammalian transcription factor ATF4 (12).”
• Translational control in the endoplasmic reticulum stress response. (2002, background): “It is also important to point out that, on balance, the ISR seems more concerned with promoting survival of stressed cells than with affecting death, particularly in light of evidence that Perk–/– knockout and eIF2αS51A knock-in cells are hypersensitive to ER stress despite their inability to induce”
• A trip to the ER: coping with stress. (2004, background): “mice and mice homozygous for phosphorylation-incompetent eIF2a display impaired physiological glucose and insulin regulation, as well as overt diabetes reminiscent of Type I diabetes in humans [56, 57 ].”
• Endoplasmic reticulum stress in disease pathogenesis. (2008, background): “In agreement with this interpretation, mice engineered to have a non-phosphorylable form of eIF2α also develop diabetes (46), as PERK decreases the load on the ER by inactivating eIF2α via Lin et al.”
• The impact of the unfolded protein response on human disease (2012, background): “The PERK–eIF2 arm of the UPR is indispensable for  cells to adapt to large fluctuations in proinsulin synthesis (Harding et al., 2000b; Scheuner et al., 2001).”