PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress

By T. Verfaillie, N. Rubio, Abhishek D Garg, G. Bultynck, R. Rizzuto, J. Decuypere, J. Piette, C. Linehan, S. Gupta, Afshin Samali and 1 more. Cell Death and Differentiation, 2012

816 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d6f02193d2e5cfd720c84c938ea229508593a5d2

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. L. Galluzzi
2. S. S. Cao
3. Guido Kroemer
4. Douglas R. Green
5. R. Kaufman
6. J. Malhotra
7. G. Hotamışlıgil
8. D. Ron

In Epidemiology

1. Guido Kroemer
2. L. Galluzzi
3. Douglas R. Green
4. Peter Vandenabeele
5. S. S. Cao
6. R. Kaufman
7. Beth Levine
8. V. Deretic

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. Douglas R. Green
4. Peter Vandenabeele
5. S. S. Cao
6. R. Kaufman
7. Beth Levine
8. Jerry M. Adams

Citations in the corpus

• Immunogenic cell death and DAMPs in cancer therapy (2012, background): “These authors showed that a recombinant N-terminal fragment of CRT (39-272) is a potent inducer of activation and maturation of B cells and macrophages and can trigger Ig class switching in B cells without T cell help in vitro and in vivo72.”
• Metabolic control of cell death (2014, background): “stores, appears to be enhanced in PERK-deficient cells (89).”
• Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease (2014, background): “Additionally, the ER stress sensor PERK resides in MAMs and helps maintain the ER-mitochondria junction that plays a critical role in mitochondrial dysfunction and apoptosis (174).”