From acute ER stress to physiological roles of the Unfolded Protein Response

By Jun Wu, R. Kaufman. Cell Death and Differentiation, 2006

942 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Surgery

View Paper: https://www.semanticscholar.org/paper/ffc8d58209506bcc2ef9a78474fbdb8a07e65fdd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. R. Kaufman
2. J. Malhotra
3. Laurie H. Glimcher
4. Ann-Hwee Lee
5. Herbert Tilg
6. A. Kaser
7. R. Blumberg
8. H. Chae

In Epidemiology

1. R. Kaufman
2. Laurie H. Glimcher
3. J. Malhotra
4. Ann-Hwee Lee
5. Herbert Tilg
6. M. Komatsu
7. H. Chae
8. Hyung-Ryong Kim

In Surgery

1. J. Malhotra
2. R. Kaufman
3. Laurie H. Glimcher
4. A. Kaser
5. R. Blumberg
6. P. Ferré
7. F. Foufelle
8. Herbert Tilg

Citations in the corpus

• Hepatic steatosis: a role for de novo lipogenesis and the transcription factor SREBP‐1c (2010, background): “Once activated, these three effectors decrease protein translation and promote expression of foldases and chaperones or proteins involved in the degradation of misfolded proteins [63,64].”
• The endoplasmic reticulum and the unfolded protein response. (2007, background): “Coordinate regulation of all these processes is required to restore proper protein folding and ER homeostasis [1-6].”
• Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, positive): “Coordinate regulation of all these processes is required to restore proper protein folding and ER homeostasis (40, 63, 86, 107, 122, 150).”
• ER stress: Autophagy induction, inhibition and selection (2015, background): “Finally, programmed cell execution is initiated when stress exceeds a given threshold and the ER is so severely impaired that compensatory mechanisms are no longer able to sustain its function.(6,7) Although ER stress and autophagy can function independently, they share a number of common features i”
• Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia. (2008, background): “, 2007; see EM pictures below) may also play a role in the increased apoptosis and decreased proliferation of b cells observed in Atg7 cell mice (Harding et al., 2001; Wu and Kaufman, 2006; Zhang et al., 2006).”
• XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease (2008, positive): “Three distinct UPR signaling pathways exist in mammalian cells that include ER transmembrane inositol-requiring enzyme 1a and b (IRE1a and b), pancreatic ER kinase (PERK), and activating transcription fac- tor 6 (ATF6) (Wu and Kaufman, 2006).”